The Link Between Obesity and Diabetes
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This review investigates the link between obesity and diabetes, providing information on the association between obesity and diabetes in order to provide effective interventions that are based on cause to effect.
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Running head: Obesity and Diabetes 1
The Link Between Obesity and Diabetes
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The Link Between Obesity and Diabetes
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Running head: Obesity and Diabetes 2
Table of Contents
ABSTRACT...............................................................................................................................3
CHATPER ONE: INTRODUCTION........................................................................................4
1.1 Background Information..................................................................................................4
1.2 Descriptive Epidemiology................................................................................................5
CHAPTER TWO: METHODS USED TO CONDUCT A SYSTEMATIC LITERATURE
REVIEW....................................................................................................................................6
2.1 Inclusion and Exclusion Criteria......................................................................................6
2.2 Key Search Terms............................................................................................................6
CHAPTER THREE: RESULTS OF THE SYSTEMATIC LITERATURE REVIEW.............7
3.1 Theoretical Models...........................................................................................................7
3.1.1 Accelerator Hypothesis..............................................................................................7
3.1.2 Excessive FFAs and Ectopic Fat-Storage Syndrome................................................7
3.1.3 Gut Microbiota and the Development of Obesity and Type 2 Diabetes....................8
3.1.4 Severe Inflammation and the Activation of the Immune System..............................9
3.1.5 Occupational Risk and Lifestyle Factors...................................................................9
3.2 Methodologies Used.......................................................................................................10
3.3 Synthesis of Research Findings......................................................................................11
CHAPTER FOUR: DISCUSSION..........................................................................................16
4.1 Brief Summary of Main Findings...................................................................................16
4.2 Strengths and Limitations of Systematic Literature Review..........................................17
4.2.1 Limitations...............................................................................................................17
4.2.2 Strengths..................................................................................................................17
4.2.3 Policy Implications..................................................................................................17
4.2.4 Key Stakeholders.....................................................................................................18
4.2.5 Recommendations for Future Research...................................................................18
CONCLUSION........................................................................................................................19
References................................................................................................................................20
Appendix: Matrix Table for Literature Review.......................................................................26
Table of Contents
ABSTRACT...............................................................................................................................3
CHATPER ONE: INTRODUCTION........................................................................................4
1.1 Background Information..................................................................................................4
1.2 Descriptive Epidemiology................................................................................................5
CHAPTER TWO: METHODS USED TO CONDUCT A SYSTEMATIC LITERATURE
REVIEW....................................................................................................................................6
2.1 Inclusion and Exclusion Criteria......................................................................................6
2.2 Key Search Terms............................................................................................................6
CHAPTER THREE: RESULTS OF THE SYSTEMATIC LITERATURE REVIEW.............7
3.1 Theoretical Models...........................................................................................................7
3.1.1 Accelerator Hypothesis..............................................................................................7
3.1.2 Excessive FFAs and Ectopic Fat-Storage Syndrome................................................7
3.1.3 Gut Microbiota and the Development of Obesity and Type 2 Diabetes....................8
3.1.4 Severe Inflammation and the Activation of the Immune System..............................9
3.1.5 Occupational Risk and Lifestyle Factors...................................................................9
3.2 Methodologies Used.......................................................................................................10
3.3 Synthesis of Research Findings......................................................................................11
CHAPTER FOUR: DISCUSSION..........................................................................................16
4.1 Brief Summary of Main Findings...................................................................................16
4.2 Strengths and Limitations of Systematic Literature Review..........................................17
4.2.1 Limitations...............................................................................................................17
4.2.2 Strengths..................................................................................................................17
4.2.3 Policy Implications..................................................................................................17
4.2.4 Key Stakeholders.....................................................................................................18
4.2.5 Recommendations for Future Research...................................................................18
CONCLUSION........................................................................................................................19
References................................................................................................................................20
Appendix: Matrix Table for Literature Review.......................................................................26
Running head: Obesity and Diabetes 3
ABSTRACT
Background: The increase in the prevalence of obesity and diabetes in both adults and
children is alarming. Studies attribute this prevalence to behavioural changes. However, there
is need for more information on the association between obesity and diabetes in order to
provide effective interventions that are based on cause to effect. This review aims at
investigating the link between obesity and diabetes.
Methods: A systematic literature review on the link between obesity and diabetes was carried
out. A total of fifteen articles published within five years were included in the assessment.
Seven of the reviewed articles were primary articles while the other eight were literature
reviews.
Results: There is a strong association between obesity and diabetes. This can be attributed to
the effect of body weight on insulin resistance and beta cell dysfunction. Insulin sensitivity is
affected bay lifestyle behaviours such as physical activity and sleep, but obesity is the leading
factor that influences the manifestation of metabolic diseases. Both T2D and obesity are
characteristic of elevated production levels of NEFAs which is also linked to insulin
resistance in both cases. Fat distribution, dysfunction of beta cells, BMI at any level of weight
gain, Excessive FFAs and ectopic fat storage, and Gut microbiota are all linked to insulin
resistance and ultimately to the development of diabetes.
Conclusion: Obesity is the most substantial risk factor for the manifestation of diabetes. The
current study identified the mechanisms in which obesity influences both type 1 and type 2
diabetes.
ABSTRACT
Background: The increase in the prevalence of obesity and diabetes in both adults and
children is alarming. Studies attribute this prevalence to behavioural changes. However, there
is need for more information on the association between obesity and diabetes in order to
provide effective interventions that are based on cause to effect. This review aims at
investigating the link between obesity and diabetes.
Methods: A systematic literature review on the link between obesity and diabetes was carried
out. A total of fifteen articles published within five years were included in the assessment.
Seven of the reviewed articles were primary articles while the other eight were literature
reviews.
Results: There is a strong association between obesity and diabetes. This can be attributed to
the effect of body weight on insulin resistance and beta cell dysfunction. Insulin sensitivity is
affected bay lifestyle behaviours such as physical activity and sleep, but obesity is the leading
factor that influences the manifestation of metabolic diseases. Both T2D and obesity are
characteristic of elevated production levels of NEFAs which is also linked to insulin
resistance in both cases. Fat distribution, dysfunction of beta cells, BMI at any level of weight
gain, Excessive FFAs and ectopic fat storage, and Gut microbiota are all linked to insulin
resistance and ultimately to the development of diabetes.
Conclusion: Obesity is the most substantial risk factor for the manifestation of diabetes. The
current study identified the mechanisms in which obesity influences both type 1 and type 2
diabetes.
Running head: Obesity and Diabetes 4
CHATPER ONE: INTRODUCTION
1.1 Background Information
Diabetes mellitus (DM) is a chronic disease that is capable of changing the metabolism of
protein, carbohydrate and fat. The disorder is a result of the unavailability of insulin secretion
caused by the inability of the beta Langerhans islet cells found in the pancreas to secrete
insulin, or it’s caused by the complications in the uptake of insulin in the proximal body
tissues. DM is further categorised into two groups namely type 1 and type 2 diabetes (Kahn,
Cooper, & Del Prato, 2014). Type 1 diabetes (T1D) is most prevalent in children, however it
can sometimes occur in adults, especially those age thirty years and above. It is commonly
the case that type 1 diabetic patients are not obese but are often diagnosed with diabetes
ketoacidosis which is an emergency status (American Diabetes Association, 2014).
The pathophysiology of type 1 diabetes shows that it is an autoimmunity (Stankov, Benc, &
Draskovic, 2013). The prevalence of type 1 diabetes is highest in the presence of other
autoimmune diseases such as Addison’s disease. The pathophysiology and aetiology of type
2 diabetes (T2D) is rather different from type 1 diabetes. The prevalence of type 2 diabetes
increases with the increasing presence of diabetes among other factors associated with it such
as physical inactivity, unhealthy diet, and urbanization (Tai, Wong, & Wen, 2015).
The increasing cases of obesity in both adults and children have been associated with the
corresponding rise in the incidence of type 2 diabetes (Bhupathiraju, & Hu, 2016). On the
other hand, the specific mechanism which leads to the increased prevalence of type 1 diabetes
is still under investigation. However, studies have shown that it is as a result of both
environmental and genetic factors (Atkinson, Eisenbarth, & Michels, 2014). Other studies
have also found out that there is a relationship between type 1 diabetes and weight gain
(Baidal et al., 2016). There is a strong relationship between obesity and type 2 diabetes which
are both related with insulin resistance. Type 2 diabetes is characteristic of endothelial
CHATPER ONE: INTRODUCTION
1.1 Background Information
Diabetes mellitus (DM) is a chronic disease that is capable of changing the metabolism of
protein, carbohydrate and fat. The disorder is a result of the unavailability of insulin secretion
caused by the inability of the beta Langerhans islet cells found in the pancreas to secrete
insulin, or it’s caused by the complications in the uptake of insulin in the proximal body
tissues. DM is further categorised into two groups namely type 1 and type 2 diabetes (Kahn,
Cooper, & Del Prato, 2014). Type 1 diabetes (T1D) is most prevalent in children, however it
can sometimes occur in adults, especially those age thirty years and above. It is commonly
the case that type 1 diabetic patients are not obese but are often diagnosed with diabetes
ketoacidosis which is an emergency status (American Diabetes Association, 2014).
The pathophysiology of type 1 diabetes shows that it is an autoimmunity (Stankov, Benc, &
Draskovic, 2013). The prevalence of type 1 diabetes is highest in the presence of other
autoimmune diseases such as Addison’s disease. The pathophysiology and aetiology of type
2 diabetes (T2D) is rather different from type 1 diabetes. The prevalence of type 2 diabetes
increases with the increasing presence of diabetes among other factors associated with it such
as physical inactivity, unhealthy diet, and urbanization (Tai, Wong, & Wen, 2015).
The increasing cases of obesity in both adults and children have been associated with the
corresponding rise in the incidence of type 2 diabetes (Bhupathiraju, & Hu, 2016). On the
other hand, the specific mechanism which leads to the increased prevalence of type 1 diabetes
is still under investigation. However, studies have shown that it is as a result of both
environmental and genetic factors (Atkinson, Eisenbarth, & Michels, 2014). Other studies
have also found out that there is a relationship between type 1 diabetes and weight gain
(Baidal et al., 2016). There is a strong relationship between obesity and type 2 diabetes which
are both related with insulin resistance. Type 2 diabetes is characteristic of endothelial
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Running head: Obesity and Diabetes 5
dysfunction which has also been associated with insulin resistance or obesity. Weight gain
and insulin resistance causes type 2 diabetes due to the inability of beta cells to fully
compensate for the poor insulin sensitivity (Ye, 2013).
1.2 Descriptive Epidemiology
Diabetes and obesity have not only reached epidemic levels but have become public health
issues in the United States and worldwide. Global statistics indicate that obesity is a much
bigger problem than hunger, and the major cause of morbidity and death across the globe
with this state of conditions expected to increase in the future. Almost one out of 10 adults in
the US have diabetes with 90% of these being diagnosed with type 2 diabetes. It has
historically been assumed that diabetes is an adult disorder, but the recent rise in body weight
in children and young adults have led to the rise in the type 2 diabetes cases, more so among
the Hispanic young adults (46.1%) and Blacks (57.8%) (Menke, Casagrande, Geiss, &
Cowie, 2015). The management and treatment of obesity and diabetes is too costly
(American Diabetes Association, 2013). The healthcare expenses for obese patients is higher
by 42% compared to those of normal-weight, whereas it is double the rate for diabetic
patients compared to non-diabetic individuals (Mozaffarian et al., 2015). Both diabetes and
obesity are correlated, intricate disorders which can significantly be prevented and treated
(Ley, Hamdy, Mohan, & Hu, 2014). Both diseases increases the risk for cardiovascular
illnesses and cerebrovascular accident. Owing to the cost and increasing incidences of both
diabetes and obesity cases across the globe, it is important that critical analysis is done on the
studies that explore the association between the two conditions. This paper provides a critical
review of modern literature on the links between obesity and diabetes.
dysfunction which has also been associated with insulin resistance or obesity. Weight gain
and insulin resistance causes type 2 diabetes due to the inability of beta cells to fully
compensate for the poor insulin sensitivity (Ye, 2013).
1.2 Descriptive Epidemiology
Diabetes and obesity have not only reached epidemic levels but have become public health
issues in the United States and worldwide. Global statistics indicate that obesity is a much
bigger problem than hunger, and the major cause of morbidity and death across the globe
with this state of conditions expected to increase in the future. Almost one out of 10 adults in
the US have diabetes with 90% of these being diagnosed with type 2 diabetes. It has
historically been assumed that diabetes is an adult disorder, but the recent rise in body weight
in children and young adults have led to the rise in the type 2 diabetes cases, more so among
the Hispanic young adults (46.1%) and Blacks (57.8%) (Menke, Casagrande, Geiss, &
Cowie, 2015). The management and treatment of obesity and diabetes is too costly
(American Diabetes Association, 2013). The healthcare expenses for obese patients is higher
by 42% compared to those of normal-weight, whereas it is double the rate for diabetic
patients compared to non-diabetic individuals (Mozaffarian et al., 2015). Both diabetes and
obesity are correlated, intricate disorders which can significantly be prevented and treated
(Ley, Hamdy, Mohan, & Hu, 2014). Both diseases increases the risk for cardiovascular
illnesses and cerebrovascular accident. Owing to the cost and increasing incidences of both
diabetes and obesity cases across the globe, it is important that critical analysis is done on the
studies that explore the association between the two conditions. This paper provides a critical
review of modern literature on the links between obesity and diabetes.
Running head: Obesity and Diabetes 6
CHAPTER TWO: METHODS USED TO CONDUCT A SYSTEMATIC
LITERATURE REVIEW
2.1 Inclusion and Exclusion Criteria
The researcher critically investigated appropriate articles and books relevant to the study
topic. Search engines like Google Scholar, PubMed, PMC, and BMC to carry out a
systematic research to find out the studies that focused on diabetes and obesity. The search
was only restricted to articles published within five years. The articles had to be on the link
between diabetes and obesity. 80 studies were retrieved from the databases after
identification, screening, and quality check. 50 articles were then included for assessment. 10
articles were not included due to duplication. Out of the 40 remaining articles, fifteen of them
were being sold and thus did not have open access. Further suitability assessment led to the
exclusion of ten more studies leaving the researcher with fifteen articles that fully met the
inclusion criteria. Among the fifteen articles, eight of them were literature reviews and the
other seven were primary articles. As a result of the critical review, different themes were
ascertained such as theoretical models, research methodologies, and the synthesis of the
findings as shown in the literature section of this paper.
2.2 Key Search Terms
The key search terms used during the research include obesity, diabetes mellitus, type 1
diabetes, type 2 diabetes, diabetes management, diabetes prevention, insulin resistance, and
prevalence.
CHAPTER TWO: METHODS USED TO CONDUCT A SYSTEMATIC
LITERATURE REVIEW
2.1 Inclusion and Exclusion Criteria
The researcher critically investigated appropriate articles and books relevant to the study
topic. Search engines like Google Scholar, PubMed, PMC, and BMC to carry out a
systematic research to find out the studies that focused on diabetes and obesity. The search
was only restricted to articles published within five years. The articles had to be on the link
between diabetes and obesity. 80 studies were retrieved from the databases after
identification, screening, and quality check. 50 articles were then included for assessment. 10
articles were not included due to duplication. Out of the 40 remaining articles, fifteen of them
were being sold and thus did not have open access. Further suitability assessment led to the
exclusion of ten more studies leaving the researcher with fifteen articles that fully met the
inclusion criteria. Among the fifteen articles, eight of them were literature reviews and the
other seven were primary articles. As a result of the critical review, different themes were
ascertained such as theoretical models, research methodologies, and the synthesis of the
findings as shown in the literature section of this paper.
2.2 Key Search Terms
The key search terms used during the research include obesity, diabetes mellitus, type 1
diabetes, type 2 diabetes, diabetes management, diabetes prevention, insulin resistance, and
prevalence.
Running head: Obesity and Diabetes 7
CHAPTER THREE: RESULTS OF THE SYSTEMATIC LITERATURE REVIEW
3.1 Theoretical Models
The researcher ascertained several theories which explain the relationship between diabetes
and obesity or weight gain.
3.1.1 Accelerator Hypothesis
The study by Al-Goblan, Al-Alfi, and Khan (2014) examined the accelerator hypothesis and
found a significant association between diabetes and obesity. The authors ascertained that the
risk of developing type 1 diabetes was significantly associated with weight gain among
youths. This is because the increase in body weight fosters insulin resistance, thus causing the
development of type 1 diabetes in people who are genetically predisposed to diabetes.
Similarly, type 2 diabetes and obesity are linked to insulin resistance because of the inability
of the beta cells to fully compensate for the low insulin sensitivity. Obesity or insulin
resistance in pre-diabetes or diabetic conditions are influenced by the endothelial dysfunction.
3.1.2 Excessive FFAs and Ectopic Fat-Storage Syndrome
Saboor Aftab, Reddy, Smith, and Barber (2014) theorised that overall and abdominal
adiposity is closely related to the development of T2D, pointing out to the significance of
waist diameter in clinical evaluation (Scott et al., 2014). Factors such as abdominal obesity,
BMI measurement, and sagittal abdominal diameter are implications for the primary role of
central adiposity in the development of T2D (Pajunen et al., 2013). High levels of visceral fat
leads to excessive production of free fatty acids (FFAs) which end up reaching the liver
through the portal vein causing fatty liver. This condition is linked to increased levels of non-
esterified fatty acid (NEFA) in the plasma which consequently leads to insulin resistance
through the Randle’s effect in the proximal body tissues such as muscles which are also the
targets of insulin (Byrne, & Targher, 2014; Ye, 2013). In the hypothesis of ectopic fat
storage, there seems to exist a depot limit for the visceral tissue, outside which the expanding
depot of the adipose tissue cannot properly store the increased fat (Choe, Huh, Hwang, Kim,
CHAPTER THREE: RESULTS OF THE SYSTEMATIC LITERATURE REVIEW
3.1 Theoretical Models
The researcher ascertained several theories which explain the relationship between diabetes
and obesity or weight gain.
3.1.1 Accelerator Hypothesis
The study by Al-Goblan, Al-Alfi, and Khan (2014) examined the accelerator hypothesis and
found a significant association between diabetes and obesity. The authors ascertained that the
risk of developing type 1 diabetes was significantly associated with weight gain among
youths. This is because the increase in body weight fosters insulin resistance, thus causing the
development of type 1 diabetes in people who are genetically predisposed to diabetes.
Similarly, type 2 diabetes and obesity are linked to insulin resistance because of the inability
of the beta cells to fully compensate for the low insulin sensitivity. Obesity or insulin
resistance in pre-diabetes or diabetic conditions are influenced by the endothelial dysfunction.
3.1.2 Excessive FFAs and Ectopic Fat-Storage Syndrome
Saboor Aftab, Reddy, Smith, and Barber (2014) theorised that overall and abdominal
adiposity is closely related to the development of T2D, pointing out to the significance of
waist diameter in clinical evaluation (Scott et al., 2014). Factors such as abdominal obesity,
BMI measurement, and sagittal abdominal diameter are implications for the primary role of
central adiposity in the development of T2D (Pajunen et al., 2013). High levels of visceral fat
leads to excessive production of free fatty acids (FFAs) which end up reaching the liver
through the portal vein causing fatty liver. This condition is linked to increased levels of non-
esterified fatty acid (NEFA) in the plasma which consequently leads to insulin resistance
through the Randle’s effect in the proximal body tissues such as muscles which are also the
targets of insulin (Byrne, & Targher, 2014; Ye, 2013). In the hypothesis of ectopic fat
storage, there seems to exist a depot limit for the visceral tissue, outside which the expanding
depot of the adipose tissue cannot properly store the increased fat (Choe, Huh, Hwang, Kim,
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Running head: Obesity and Diabetes 8
& Kim, 2016; Boren, Taskinen, Olofsson, & Levin, 2013). As a result, the excess fat is
deposited in the sites of extra adipose tissue such as skeletal muscles, liver among others,
leading to elevated levels of insulin resistance, damaged function of the beta cells and finally
T2D (Lafontan, 2014; Rutkowski, Stern, & Scherer, 2015). Vasques et al. (2015) also found
out that sagittal abdominal circumference could be used as a predictor of insulin resistance
among people of different ethnicities.
The adipocytokines are also believed to be instrumental in the development of T2D that is
associated with obesity. The obese adults undergo expansion of fat mass which causes the
adipocytes to secret fatty acids, different adipocytokines and inflammation of mediators
(McGown, Birerdinc, & Younossi, 2014; Blüher,2014). The adipose tissue then responds to
the varying nutrient and neuro-hormonal indicators by producing adipocytokines that regulate
eating, immunity, and thermogenesis. Consequently, the sensitivity of insulin towards the
various organs of target are altered by the adipocytokines, and thus leading to obesity which
is associated with T2D (Nakamura, Fuster, & Walsh, 2014; Smitka, & Marešová, 2015).
3.1.3 Gut Microbiota and the Development of Obesity and Type 2 Diabetes
There is evidence of a strong relationship between gut microbiota and the development of
obesity by influencing different factors such as increasing food intake, intestinal
permeability, and inflammation among others (Devaraj, Hemarajata, & Versalovic, 2013;
Naseer et al., 2014). This theory is based on the findings that some types of bacteria
belonging to the gut microbiota are actively responsible for the uptake of nutrients and
dispensing energy. Whereas the lipopolysaccharide (LPS) which is secreted in the gut which
is home to several microbes may be an inducing element and linking inflammation to the
unhealthy diet characteristic of excess fats which causes obesity (Devaraj, Hemarajata, &
Versalovic, 2013). The gut microorganisms increase the absorption of monosaccharide from
& Kim, 2016; Boren, Taskinen, Olofsson, & Levin, 2013). As a result, the excess fat is
deposited in the sites of extra adipose tissue such as skeletal muscles, liver among others,
leading to elevated levels of insulin resistance, damaged function of the beta cells and finally
T2D (Lafontan, 2014; Rutkowski, Stern, & Scherer, 2015). Vasques et al. (2015) also found
out that sagittal abdominal circumference could be used as a predictor of insulin resistance
among people of different ethnicities.
The adipocytokines are also believed to be instrumental in the development of T2D that is
associated with obesity. The obese adults undergo expansion of fat mass which causes the
adipocytes to secret fatty acids, different adipocytokines and inflammation of mediators
(McGown, Birerdinc, & Younossi, 2014; Blüher,2014). The adipose tissue then responds to
the varying nutrient and neuro-hormonal indicators by producing adipocytokines that regulate
eating, immunity, and thermogenesis. Consequently, the sensitivity of insulin towards the
various organs of target are altered by the adipocytokines, and thus leading to obesity which
is associated with T2D (Nakamura, Fuster, & Walsh, 2014; Smitka, & Marešová, 2015).
3.1.3 Gut Microbiota and the Development of Obesity and Type 2 Diabetes
There is evidence of a strong relationship between gut microbiota and the development of
obesity by influencing different factors such as increasing food intake, intestinal
permeability, and inflammation among others (Devaraj, Hemarajata, & Versalovic, 2013;
Naseer et al., 2014). This theory is based on the findings that some types of bacteria
belonging to the gut microbiota are actively responsible for the uptake of nutrients and
dispensing energy. Whereas the lipopolysaccharide (LPS) which is secreted in the gut which
is home to several microbes may be an inducing element and linking inflammation to the
unhealthy diet characteristic of excess fats which causes obesity (Devaraj, Hemarajata, &
Versalovic, 2013). The gut microorganisms increase the absorption of monosaccharide from
Running head: Obesity and Diabetes 9
the intestinal tract and trigger the host to increase the hepatic secretion of triglycerides. This
activity fosters elevated levels of insulin resistance (Mikkelsen et al., 2015).
3.1.4 Severe Inflammation and the Activation of the Immune System
Esser, Legrand-Poels, Piette, Scheen, and Paquot (2014) theorised that severe inflammation
and the activation of the immune system triggers insulin resistance which is associated to
both T2D and obesity. The common sites of inflammation in obese cases include the muscles,
liver, and adipose tissue. The permeation of some immune cells and macrophages takes place
in these organs causing a shift in cell population which enhances inflammation. These cells
are vital in the secretion of cytokines which encourage inflammation and thus altering the
signalling of insulin in the proximal tissues or trigger the dysfunction of beta cells leading to
inadequate insulin.
Obesity which leads to type 1 diabetes is as a result of lack of physical activity. Being
physically active increases fitness in people with T1D, however the decreased fitness level in
youths is an indication of low aerobic power and strength. The routine involvement in
physical activities is enhances lipid levels, insulin resistance, and endothelial function, with
the exception of blood pressure in people with type 1 diabetes (Minges, Whittemore, & Grey,
2013; Liese, Ma, Maahs, & Trilk, 2013).
3.1.5 Occupational Risk and Lifestyle Factors
Poulsen, Cleal, Clausen, and Andersen (2014) found out that both occupational risk and
lifestyle factors were influential in developing diabetes. BMI above the normal body weight
is the most significant risk factor. Furthermore, overweight is related with physical inactivity,
shift work, and issues to do with sleep and health. According to Ganz, Wintfeld, Li, Alas,
Langer and Hammer (2014) there is a strong independent association between BMI and the
risk of developing T2D. The higher the BMI the higher the chances of being diagnosed with
T2D. Metabolic syndrome is high among employees due to their nature of lifestyle which is
the intestinal tract and trigger the host to increase the hepatic secretion of triglycerides. This
activity fosters elevated levels of insulin resistance (Mikkelsen et al., 2015).
3.1.4 Severe Inflammation and the Activation of the Immune System
Esser, Legrand-Poels, Piette, Scheen, and Paquot (2014) theorised that severe inflammation
and the activation of the immune system triggers insulin resistance which is associated to
both T2D and obesity. The common sites of inflammation in obese cases include the muscles,
liver, and adipose tissue. The permeation of some immune cells and macrophages takes place
in these organs causing a shift in cell population which enhances inflammation. These cells
are vital in the secretion of cytokines which encourage inflammation and thus altering the
signalling of insulin in the proximal tissues or trigger the dysfunction of beta cells leading to
inadequate insulin.
Obesity which leads to type 1 diabetes is as a result of lack of physical activity. Being
physically active increases fitness in people with T1D, however the decreased fitness level in
youths is an indication of low aerobic power and strength. The routine involvement in
physical activities is enhances lipid levels, insulin resistance, and endothelial function, with
the exception of blood pressure in people with type 1 diabetes (Minges, Whittemore, & Grey,
2013; Liese, Ma, Maahs, & Trilk, 2013).
3.1.5 Occupational Risk and Lifestyle Factors
Poulsen, Cleal, Clausen, and Andersen (2014) found out that both occupational risk and
lifestyle factors were influential in developing diabetes. BMI above the normal body weight
is the most significant risk factor. Furthermore, overweight is related with physical inactivity,
shift work, and issues to do with sleep and health. According to Ganz, Wintfeld, Li, Alas,
Langer and Hammer (2014) there is a strong independent association between BMI and the
risk of developing T2D. The higher the BMI the higher the chances of being diagnosed with
T2D. Metabolic syndrome is high among employees due to their nature of lifestyle which is
Running head: Obesity and Diabetes 10
sedentary. This can be attributed to the socioeconomic changes and transitions in diet among
employees. Overweight is the leading metabolic syndrome among employees of North East
China in both genders (Wang et al., 2015). Pulgaron and Delamater (2014) studied obesity
and diabetes in children and demonstrates that factors such as individual history of obesity,
culture, environment and genetic are attributed to obesity risk. Costa et al. (2016) also found
out that the prevalence of obese cases in T1D children was highly associated with lifestyle
behavioural factors such as consumption of unhealthy foods, low socioeconomic activities,
and overfeeding from parents due to fear of hypoglycaemia. Bhupathiraju and Hu (2016)
opined that abdominal obesity, changes in agricultural policies, trends in physical activity and
napping, dietary changes, and genetics are the factors that foster obesity and diabetes.
3.2 Methodologies Used
Al-Goblan et al. (2014) conducted a literature review on the association between obesity and
insulin resistance (diabetes mellitus). A review was similarly conducted by Saboor Aftab et
al. (2014) on the complex relation between obesity and type 2 diabetes. Reviews on the
function of the Gut microbiota in diabetes and obesity were conducted by Naseer et al. (2014)
and Devaraj et al. (2013). Another literature review was conducted on the association
between inflammation and obesity, T2D, and metabolic syndrome by Esser et al. (2013).
Minges et al. (2013) used a systematic literature review to assess the link between physical
activity, nutrition, sleep, and sedentary lifestyle and obesity in young adults diagnosed with
type 1 diabetes. A literature review was also conducted by Pulgaron and Delamater (2014) on
obesity and T2D in children.
Vasques et al. (2015) used a multicentre population survey to ascertain whether sagittal
abdominal diameter could be used as a predictor of insulin resistance. Poulsen et al. (2014)
conducted a prospective cohort study using questionnaire to explore the relationship between
job, obesity and diabetes. A case control study was used by Ganz et al. (2014) to ascertain the
sedentary. This can be attributed to the socioeconomic changes and transitions in diet among
employees. Overweight is the leading metabolic syndrome among employees of North East
China in both genders (Wang et al., 2015). Pulgaron and Delamater (2014) studied obesity
and diabetes in children and demonstrates that factors such as individual history of obesity,
culture, environment and genetic are attributed to obesity risk. Costa et al. (2016) also found
out that the prevalence of obese cases in T1D children was highly associated with lifestyle
behavioural factors such as consumption of unhealthy foods, low socioeconomic activities,
and overfeeding from parents due to fear of hypoglycaemia. Bhupathiraju and Hu (2016)
opined that abdominal obesity, changes in agricultural policies, trends in physical activity and
napping, dietary changes, and genetics are the factors that foster obesity and diabetes.
3.2 Methodologies Used
Al-Goblan et al. (2014) conducted a literature review on the association between obesity and
insulin resistance (diabetes mellitus). A review was similarly conducted by Saboor Aftab et
al. (2014) on the complex relation between obesity and type 2 diabetes. Reviews on the
function of the Gut microbiota in diabetes and obesity were conducted by Naseer et al. (2014)
and Devaraj et al. (2013). Another literature review was conducted on the association
between inflammation and obesity, T2D, and metabolic syndrome by Esser et al. (2013).
Minges et al. (2013) used a systematic literature review to assess the link between physical
activity, nutrition, sleep, and sedentary lifestyle and obesity in young adults diagnosed with
type 1 diabetes. A literature review was also conducted by Pulgaron and Delamater (2014) on
obesity and T2D in children.
Vasques et al. (2015) used a multicentre population survey to ascertain whether sagittal
abdominal diameter could be used as a predictor of insulin resistance. Poulsen et al. (2014)
conducted a prospective cohort study using questionnaire to explore the relationship between
job, obesity and diabetes. A case control study was used by Ganz et al. (2014) to ascertain the
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Running head: Obesity and Diabetes 11
link between body mass index and the risk of being diagnosed with T2D. Wang et al. (2015)
carried out a health screening of employees in North East China to approximate the metabolic
syndrome (overweight, T2D) prevalence among them. An analytical cross-sectional study
was conducted on type 1 diabetes to determine the frequency of obese cases in children
diagnosed with T1D and the associated factors (Costa et al., 2016). A cohort follow-up study
was conducted on healthy young adults to ascertain the incidence of diabetes overtime (Twig
et al., 2014). Lukács, Kiss-Tóth, Csordás, Sasvári, and Barkai (2018) conducted a population
based quantitative study to assess the associated risks of T2D in adolescent students
diagnosed with overweight and obesity.
3.3 Synthesis of Research Findings
A literature review on the association between obesity and insulin resistance was conducted
by Al-Goblan et al. (2014). The authors found out that there was a significant association
between BMI and diabetes and insulin resistance. The findings indicate that there is an
increase in the quantities of glycerol hormones, NEFA, among other substances that are
active in the development of insulin resistance in obese people. Furthermore, the impairment
of the function of beta cells alongside insulin resistance causes diabetes development.
Excessive weight at an early age is related to development of T1D. The authors also found
out that NEFA was key in the initiation of insulin resistance and in the compromise of the
functionality of beta cell.
Saboor Aftab et al. (2014) carried out a literature review on obesity and T2D and found out
that diabesity is as a result of the continued and excessive intake of energy-dense foods and
physical inactivity. Excessive intake of energy-dense foods caused increased fat deposition
and fosters insulin resistance. A fatty liver is caused by the release of free fatty acids (FFA) to
the liver through the portal vein. The spill of FFA into the systemic circulation leads to
liptoxicity of body tissues such as the heart and muscles causing a viscid cycle of fat damage
link between body mass index and the risk of being diagnosed with T2D. Wang et al. (2015)
carried out a health screening of employees in North East China to approximate the metabolic
syndrome (overweight, T2D) prevalence among them. An analytical cross-sectional study
was conducted on type 1 diabetes to determine the frequency of obese cases in children
diagnosed with T1D and the associated factors (Costa et al., 2016). A cohort follow-up study
was conducted on healthy young adults to ascertain the incidence of diabetes overtime (Twig
et al., 2014). Lukács, Kiss-Tóth, Csordás, Sasvári, and Barkai (2018) conducted a population
based quantitative study to assess the associated risks of T2D in adolescent students
diagnosed with overweight and obesity.
3.3 Synthesis of Research Findings
A literature review on the association between obesity and insulin resistance was conducted
by Al-Goblan et al. (2014). The authors found out that there was a significant association
between BMI and diabetes and insulin resistance. The findings indicate that there is an
increase in the quantities of glycerol hormones, NEFA, among other substances that are
active in the development of insulin resistance in obese people. Furthermore, the impairment
of the function of beta cells alongside insulin resistance causes diabetes development.
Excessive weight at an early age is related to development of T1D. The authors also found
out that NEFA was key in the initiation of insulin resistance and in the compromise of the
functionality of beta cell.
Saboor Aftab et al. (2014) carried out a literature review on obesity and T2D and found out
that diabesity is as a result of the continued and excessive intake of energy-dense foods and
physical inactivity. Excessive intake of energy-dense foods caused increased fat deposition
and fosters insulin resistance. A fatty liver is caused by the release of free fatty acids (FFA) to
the liver through the portal vein. The spill of FFA into the systemic circulation leads to
liptoxicity of body tissues such as the heart and muscles causing a viscid cycle of fat damage
Running head: Obesity and Diabetes 12
and inflammation which worsens insulin resistance, dysfunction of beta cells and finally the
development of type 2 diabetes. Furthermore, the authors ascertained that an independent
determinant of insulin resistance is visceral fat content whereas adipokines prevent the
development of type 2 diabetes which is caused by obesity.
Naseer et al. (2014) conducted a literature review and examined the function of gut
microbiota in T2D, obesity and Alzheimer’s disease and showed that there was a relationship
between the human microbial flora and the manifestation of metabolic syndrome such as
T2D, obesity and other related illnesses. The gut microbiota regulates energy balance and
adiposity in the host through different process such as the rise in the uptake of energy from
nutrition, regulation of the composition of tissiue fatty acid, the modulation of peptides
secreted in the gut and bile acids. The microbiota gut is also influential in the metabolism of
sugar and lipid and in the LPS development which both fosters low grade inflammation in
obesity and type 2 diabetes which is obesity-based. Similar studies were conducted by
Deveraj et al. (2013) and found out that the gut microbes had a substantial positive effect on
the metabolic syndrome, diabetes and obesity. Elevated levels of FFA and hyperglycemia are
the typical features of obesity, diabetes, and metabolic syndrome, alongside a diet with excess
fat and energy dense foods. All these increasingly activates the inflamasome complex in
addition to increasing the activation of macrophages. Moreover, macrophages can penetrate
the adipose tissue and trigger mitogen-triggered protein kinases leading to elevated cross-talk
and adipokines. A diet rich in fat and hyperlgycemic one causes alterations in the gut
microbiome by changing the content of histidine among others causing dysfunction of the gut
and conditions common in diabetes, obesity and metabolic syndrome by altering the response
of the host.
and inflammation which worsens insulin resistance, dysfunction of beta cells and finally the
development of type 2 diabetes. Furthermore, the authors ascertained that an independent
determinant of insulin resistance is visceral fat content whereas adipokines prevent the
development of type 2 diabetes which is caused by obesity.
Naseer et al. (2014) conducted a literature review and examined the function of gut
microbiota in T2D, obesity and Alzheimer’s disease and showed that there was a relationship
between the human microbial flora and the manifestation of metabolic syndrome such as
T2D, obesity and other related illnesses. The gut microbiota regulates energy balance and
adiposity in the host through different process such as the rise in the uptake of energy from
nutrition, regulation of the composition of tissiue fatty acid, the modulation of peptides
secreted in the gut and bile acids. The microbiota gut is also influential in the metabolism of
sugar and lipid and in the LPS development which both fosters low grade inflammation in
obesity and type 2 diabetes which is obesity-based. Similar studies were conducted by
Deveraj et al. (2013) and found out that the gut microbes had a substantial positive effect on
the metabolic syndrome, diabetes and obesity. Elevated levels of FFA and hyperglycemia are
the typical features of obesity, diabetes, and metabolic syndrome, alongside a diet with excess
fat and energy dense foods. All these increasingly activates the inflamasome complex in
addition to increasing the activation of macrophages. Moreover, macrophages can penetrate
the adipose tissue and trigger mitogen-triggered protein kinases leading to elevated cross-talk
and adipokines. A diet rich in fat and hyperlgycemic one causes alterations in the gut
microbiome by changing the content of histidine among others causing dysfunction of the gut
and conditions common in diabetes, obesity and metabolic syndrome by altering the response
of the host.
Running head: Obesity and Diabetes 13
Likewise, Esser et al. (2014) conducted a review on the association of inflammation
between T2D, obesity and metabolic syndrome and showed that low-grade inflammation and
a triggered immune system had a central role in the development of insulin resistance
associated to obesity and T2D. Vasques et al. (2015) carried out a survey on a women
population of multiple races to determine whether sagittal abdominal diameter (SAD) can be
used as a predictor of insulin resistance (IR). The findings indicate that there was a
substantive positive correlation between the adjusted age and total body fat mass and the BMI
with the measured IR. The women with high sagittal abdominal diameter were three times
more likely to be diagnosed with insulin resistance compares with those with normal sagittal
abdominal diameter. On the other hand, the participants with increased BMI and waist
circumference were twice more likely to have insulin resistance. The study was of clinical
relevance as it was the first to examine the use of SAD in the screening of insulin resistance
in an ethnically diverse population of adult women. However, the study did not validate SAD
as a predictor of clinical outcomes in the population of Brazil.
Minges et al. (2013) carried a systematic review to assess overweight and obesity in youth
diagnosed with T1D with a particular focus on their association with physical activity,
napping, nutrition, and sedentary lifestyle. The authors found out that overweight in T1D
youths was related to irregular sleep, too much TV watching, and skipping dinner and
breakfast, however, there was no association with physical activity. Wight management
mechanisms showed progressive weight loss alongside better glycemic control. The study
points out the existing gap in the literature on the previous studies and impacts of too much
weight gain in children diagnosed with T1D, thus prompting further research.
Poulsen et al. (2014) carried out a prospective cohort study on healthcare workers to ascertain
the association between work, obesity and diabetes. The results show that 3.5% of the
Likewise, Esser et al. (2014) conducted a review on the association of inflammation
between T2D, obesity and metabolic syndrome and showed that low-grade inflammation and
a triggered immune system had a central role in the development of insulin resistance
associated to obesity and T2D. Vasques et al. (2015) carried out a survey on a women
population of multiple races to determine whether sagittal abdominal diameter (SAD) can be
used as a predictor of insulin resistance (IR). The findings indicate that there was a
substantive positive correlation between the adjusted age and total body fat mass and the BMI
with the measured IR. The women with high sagittal abdominal diameter were three times
more likely to be diagnosed with insulin resistance compares with those with normal sagittal
abdominal diameter. On the other hand, the participants with increased BMI and waist
circumference were twice more likely to have insulin resistance. The study was of clinical
relevance as it was the first to examine the use of SAD in the screening of insulin resistance
in an ethnically diverse population of adult women. However, the study did not validate SAD
as a predictor of clinical outcomes in the population of Brazil.
Minges et al. (2013) carried a systematic review to assess overweight and obesity in youth
diagnosed with T1D with a particular focus on their association with physical activity,
napping, nutrition, and sedentary lifestyle. The authors found out that overweight in T1D
youths was related to irregular sleep, too much TV watching, and skipping dinner and
breakfast, however, there was no association with physical activity. Wight management
mechanisms showed progressive weight loss alongside better glycemic control. The study
points out the existing gap in the literature on the previous studies and impacts of too much
weight gain in children diagnosed with T1D, thus prompting further research.
Poulsen et al. (2014) carried out a prospective cohort study on healthcare workers to ascertain
the association between work, obesity and diabetes. The results show that 3.5% of the
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Running head: Obesity and Diabetes 14
respondents had manifestations of diabetes which was linked to obesity, overweight and age.
Obesity was much prevalent in the young workers and was strongly related with the
manifestation of diabetes and physical inactivity. The study confirmed that the most
influential risk factor for diabetes was obesity which was also determined by some
occupational risk factors. However, the baseline measures in this study were only based on
self-report thus raising the issue of reliability, but the large sample size in addition to the high
response rate increases the generalizability of the findings.
Ganz et al. (2014) carried out a case-control study using the electronic health database in the
US to ascertain the link between BMI and the risk of T2D.The outcomes showed a significant
positive independent association between BMI and the risk of developing type 2 diabetes.
However, the study did not assess the causal impact of BMI on the risk of developing type 2
diabetes due to the utilization of a retrospective cohort approach. Furthermore, the analysis
was only based on one integrated health system meant for Pennsylvania population thus
limiting generalizability to extensive population and in different settings.
A study on the prevalence of metabolic syndrome among North East China employees was
carried out by Wang et al. (2015). The metabolic syndrome definitions consisted of
abdominal obesity, elevated glucose fasting among others. The results indicated high
prevalence of metabolic syndrome with overweight being the most common in men (54.7%)
and women with central obesity accounting for 35.9% both of which are risk factors in the
development of diabetes. The study of Wang and colleagues is based on a large sample size
of workers in china and is the first study to scientifically investigate the incidence of
metabolic syndrome among workers of china. However, the study might have underestimated
the incidence of metabolic syndrome among the workers in Northeast China due to the
absence of information.
respondents had manifestations of diabetes which was linked to obesity, overweight and age.
Obesity was much prevalent in the young workers and was strongly related with the
manifestation of diabetes and physical inactivity. The study confirmed that the most
influential risk factor for diabetes was obesity which was also determined by some
occupational risk factors. However, the baseline measures in this study were only based on
self-report thus raising the issue of reliability, but the large sample size in addition to the high
response rate increases the generalizability of the findings.
Ganz et al. (2014) carried out a case-control study using the electronic health database in the
US to ascertain the link between BMI and the risk of T2D.The outcomes showed a significant
positive independent association between BMI and the risk of developing type 2 diabetes.
However, the study did not assess the causal impact of BMI on the risk of developing type 2
diabetes due to the utilization of a retrospective cohort approach. Furthermore, the analysis
was only based on one integrated health system meant for Pennsylvania population thus
limiting generalizability to extensive population and in different settings.
A study on the prevalence of metabolic syndrome among North East China employees was
carried out by Wang et al. (2015). The metabolic syndrome definitions consisted of
abdominal obesity, elevated glucose fasting among others. The results indicated high
prevalence of metabolic syndrome with overweight being the most common in men (54.7%)
and women with central obesity accounting for 35.9% both of which are risk factors in the
development of diabetes. The study of Wang and colleagues is based on a large sample size
of workers in china and is the first study to scientifically investigate the incidence of
metabolic syndrome among workers of china. However, the study might have underestimated
the incidence of metabolic syndrome among the workers in Northeast China due to the
absence of information.
Running head: Obesity and Diabetes 15
Pulgaron and Delamater (2014) in their literature review on the epidemiology and
management of T2D and obesity ascertained several factors that lead to the two disorders.
The authors found out that overweight in children increases the possibility of being diagnosed
with obesity in the later years. The prevalence of T2D is much higher in youths with a family
background of type 2 diabetes and obesity. Additionally, incidences of obesity and T2D are
lower in youths from lower income families and ethnic minority. Costa et al. (2016) also
assessed overweight in young adults and children diagnosed with T1D with an emphasis on
the incidence and related factors. The study found out that there was a high incidence of
overweight among the children and adolescents with T1D. This was majorly attributed to
unhealthy eating habits and sedentary lifestyle. These findings were supported by previous
studies (Meissner et al., 2014). Twig et al. (2014) also found out that the prevalence of
diabetes was linked to obesity and overweight, and the absence of diabetes risk factors and
presence of health metabolic profile were not an a safeguard against diabetes. The study was
however focused on men only thus restricting its replication in a population of women. The
quantitative study undertaken by Lukács et al. (2018) on the factors for T2D in obese and
overweight students in school indicates that the young adults are more prone to diabetes and
overweight. This study was however limited in that the screening of risk factors for the
manifestations of T2D was only done on the obese and overweight students, and yet the
disorder can take place in individuals with normal body mass.
Pulgaron and Delamater (2014) in their literature review on the epidemiology and
management of T2D and obesity ascertained several factors that lead to the two disorders.
The authors found out that overweight in children increases the possibility of being diagnosed
with obesity in the later years. The prevalence of T2D is much higher in youths with a family
background of type 2 diabetes and obesity. Additionally, incidences of obesity and T2D are
lower in youths from lower income families and ethnic minority. Costa et al. (2016) also
assessed overweight in young adults and children diagnosed with T1D with an emphasis on
the incidence and related factors. The study found out that there was a high incidence of
overweight among the children and adolescents with T1D. This was majorly attributed to
unhealthy eating habits and sedentary lifestyle. These findings were supported by previous
studies (Meissner et al., 2014). Twig et al. (2014) also found out that the prevalence of
diabetes was linked to obesity and overweight, and the absence of diabetes risk factors and
presence of health metabolic profile were not an a safeguard against diabetes. The study was
however focused on men only thus restricting its replication in a population of women. The
quantitative study undertaken by Lukács et al. (2018) on the factors for T2D in obese and
overweight students in school indicates that the young adults are more prone to diabetes and
overweight. This study was however limited in that the screening of risk factors for the
manifestations of T2D was only done on the obese and overweight students, and yet the
disorder can take place in individuals with normal body mass.
Running head: Obesity and Diabetes 16
CHAPTER FOUR: DISCUSSION
4.1 Brief Summary of Main Findings
The outcomes of the review show a strong positive significant link between obesity and
diabetes. Weight gain or diabetes is associated to diabetes by fostering insulin resistance and
the dysfunction of beta cells. The fluctuation in insulin sensitivity takes place in different
stages of life such as during pregnancy and in the process of aging. Furthermore, lifestyle
behaviours such as sleep, physical activity and elevated intake of carbohydrates also affect
the variations in insulin sensitivity. However, studies have indicated that obesity is the most
common factor that influences the manifestation of metabolic diseases. The body metabolism
is affected by the adipose tissue through hormonal secretion such as cytokines and the
secretion of NEFAs. The rate of secretion of these substances is much higher in obese people.
Insulin insensitivity is majorly impacted by the secretion of the NEFAs. Both T2D and
obesity are characteristic of elevated production levels of NEFAs which is also linked to
insulin resistance in both cases. Fat distribution is another factor which is also a determinant
of insulin sensitivity. BMI at any level of weight gain is linked to insulin resistance. In other
words, people with increased peripheral fat distribution have higher levels of insulin
sensitivity compared to those with centralised fat distribution especially in the abdomen and
chest. The dysfunction of beta cells is also associated with diabetes. Beta cells are significant
in moderating the release of insulin and the amount released is dependent on the nature,
amount and path of stimulus administration. Thus, the beta cells make sure that the
concentrations of blood sugar in health people is stabilised. The failure of the normal
communication between insulin sensitive tissues and the beta cells causes instability in
glucose levels and the development of diabetes. Excessive FFAs and ectopic fat storage are
also associated to the development of T2D. Recent studies have also associated gut
CHAPTER FOUR: DISCUSSION
4.1 Brief Summary of Main Findings
The outcomes of the review show a strong positive significant link between obesity and
diabetes. Weight gain or diabetes is associated to diabetes by fostering insulin resistance and
the dysfunction of beta cells. The fluctuation in insulin sensitivity takes place in different
stages of life such as during pregnancy and in the process of aging. Furthermore, lifestyle
behaviours such as sleep, physical activity and elevated intake of carbohydrates also affect
the variations in insulin sensitivity. However, studies have indicated that obesity is the most
common factor that influences the manifestation of metabolic diseases. The body metabolism
is affected by the adipose tissue through hormonal secretion such as cytokines and the
secretion of NEFAs. The rate of secretion of these substances is much higher in obese people.
Insulin insensitivity is majorly impacted by the secretion of the NEFAs. Both T2D and
obesity are characteristic of elevated production levels of NEFAs which is also linked to
insulin resistance in both cases. Fat distribution is another factor which is also a determinant
of insulin sensitivity. BMI at any level of weight gain is linked to insulin resistance. In other
words, people with increased peripheral fat distribution have higher levels of insulin
sensitivity compared to those with centralised fat distribution especially in the abdomen and
chest. The dysfunction of beta cells is also associated with diabetes. Beta cells are significant
in moderating the release of insulin and the amount released is dependent on the nature,
amount and path of stimulus administration. Thus, the beta cells make sure that the
concentrations of blood sugar in health people is stabilised. The failure of the normal
communication between insulin sensitive tissues and the beta cells causes instability in
glucose levels and the development of diabetes. Excessive FFAs and ectopic fat storage are
also associated to the development of T2D. Recent studies have also associated gut
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Running head: Obesity and Diabetes 17
microbiota with the development of obesity and T2D. Severe inflammation and the activation
of the immune system triggers insulin resistance which is associated to both T2D and obesity.
4.2 Strengths and Limitations of Systematic Literature Review
4.2.1 Limitations
As is always inherent with literature reviews, a number of limitations are prevalent. As much
as this study exhaustively conducted a review of current studies relevant to the study topic, it
is likely that some studies were not included in the analysis due to selection bias or
publication. Nonetheless, the findings of this review can be moderated because the researcher
did not find any extra manuscript from the searched list of reference.
4.2.2 Strengths
The review investigated current literatures of five years only. This implies that the findings
are relevant to the current trend of the diseases and thus will provide vital information to both
researchers and policy makers. The review included both reviews and primary data at the
ratio of 8:7 respectively. This is strength to the study because the findings are based on
analysis of both primary and secondary data thus increasing its credibility and findings. The
review also followed an inclusion and exclusion criteria in the selection of articles for
inclusion thus minimizing any possible selection bias. Furthermore, it ensured that only the
relevant articles are included in the analysis, thus increasing the reliability and validity of the
study. The review was not limited to any geographical setting thus increasing the possibility
of generalizing the outcomes in any population setting.
4.2.3 Policy Implications
The findings of the review have policy implications on various aspects of healthcare services.
The outcomes of the review can be a guide in policy planning and implementation in the
department of health, schools and communities due to the evidence on the association
between diet and diabetes and obesity or weight gain. Additionally, the study outcomes can
microbiota with the development of obesity and T2D. Severe inflammation and the activation
of the immune system triggers insulin resistance which is associated to both T2D and obesity.
4.2 Strengths and Limitations of Systematic Literature Review
4.2.1 Limitations
As is always inherent with literature reviews, a number of limitations are prevalent. As much
as this study exhaustively conducted a review of current studies relevant to the study topic, it
is likely that some studies were not included in the analysis due to selection bias or
publication. Nonetheless, the findings of this review can be moderated because the researcher
did not find any extra manuscript from the searched list of reference.
4.2.2 Strengths
The review investigated current literatures of five years only. This implies that the findings
are relevant to the current trend of the diseases and thus will provide vital information to both
researchers and policy makers. The review included both reviews and primary data at the
ratio of 8:7 respectively. This is strength to the study because the findings are based on
analysis of both primary and secondary data thus increasing its credibility and findings. The
review also followed an inclusion and exclusion criteria in the selection of articles for
inclusion thus minimizing any possible selection bias. Furthermore, it ensured that only the
relevant articles are included in the analysis, thus increasing the reliability and validity of the
study. The review was not limited to any geographical setting thus increasing the possibility
of generalizing the outcomes in any population setting.
4.2.3 Policy Implications
The findings of the review have policy implications on various aspects of healthcare services.
The outcomes of the review can be a guide in policy planning and implementation in the
department of health, schools and communities due to the evidence on the association
between diet and diabetes and obesity or weight gain. Additionally, the study outcomes can
Running head: Obesity and Diabetes 18
be used designing policies on dietary guidelines for populations, schools or hospitals that
have high risk of developing cardiovascular conditions
The department of health can also utilize the outcomes of the study to update its polices on
the provision of healthcare services to individuals diagnosed with cardiovascular diseases
based on the current trend in order to offer patient centred services
4.2.4 Key Stakeholders
Some of the key stakeholders to the findings of this study include the school administrations
especially in the urban schools which have been shown to be at risk of developing obesity
and diabetes. The school administration are key stakeholders because of the overwhelming
evidence of the increasing cases of diabetes and obesity in school-age youths and children.
They will find this information important in designing effective interventions
The department to health is also a potential stakeholder because its mission is to offer quality
and effective healthcare services to the citizens. This study will be of essence to the
department in designing and planning community based intervention programs aimed at
preventing and managing the increasing prevalence of diabetes and obesity.
The hospital administrations are some of the potential stakeholders because of the increasing
evidence of the effectiveness of behaviour approaches towards the prevention and
management of diabetes and obesity, which is partially addressed in this review. Thus, the
healthcare providers can be trained to integrate such approaches to the normal
pharmacological approach.
4.2.5 Recommendations for Future Research
Further studies should be conducted on how to manage and prevent diabetes and obesity
based on findings of this study. This is essential as this study considers the epidemiology and
pathophysiology of the disorders, thus necessitating an intervention that works from cause to
be used designing policies on dietary guidelines for populations, schools or hospitals that
have high risk of developing cardiovascular conditions
The department of health can also utilize the outcomes of the study to update its polices on
the provision of healthcare services to individuals diagnosed with cardiovascular diseases
based on the current trend in order to offer patient centred services
4.2.4 Key Stakeholders
Some of the key stakeholders to the findings of this study include the school administrations
especially in the urban schools which have been shown to be at risk of developing obesity
and diabetes. The school administration are key stakeholders because of the overwhelming
evidence of the increasing cases of diabetes and obesity in school-age youths and children.
They will find this information important in designing effective interventions
The department to health is also a potential stakeholder because its mission is to offer quality
and effective healthcare services to the citizens. This study will be of essence to the
department in designing and planning community based intervention programs aimed at
preventing and managing the increasing prevalence of diabetes and obesity.
The hospital administrations are some of the potential stakeholders because of the increasing
evidence of the effectiveness of behaviour approaches towards the prevention and
management of diabetes and obesity, which is partially addressed in this review. Thus, the
healthcare providers can be trained to integrate such approaches to the normal
pharmacological approach.
4.2.5 Recommendations for Future Research
Further studies should be conducted on how to manage and prevent diabetes and obesity
based on findings of this study. This is essential as this study considers the epidemiology and
pathophysiology of the disorders, thus necessitating an intervention that works from cause to
Running head: Obesity and Diabetes 19
effect. There is need for researchers to focus on providing detailed information on the
mechanisms in which varying bacterial groups in the gut can impact body metabolisms.
effect. There is need for researchers to focus on providing detailed information on the
mechanisms in which varying bacterial groups in the gut can impact body metabolisms.
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Running head: Obesity and Diabetes 20
CONCLUSION
Obesity and diabetes are some of the most prevalent illnesses that are on the increase across
the globe. This is despite of the numeral studies that have been done on the possible effective
intervention to prevent and manage the disorders. The current trend shows that both type 1
and type 2 diabetes are prevalent in both children and adults, with noticeable high incidence
among school going children and youths. This overwhelming increase in the incidences of the
disease have attracted the attention of several researches aimed at ascertaining the association
between obesity and diabetes and the corresponding risk factors. As a result, several
theoretical models have been developed on the possible association between diabetes and
obesity. These include Excessive FFAs and Ectopic fat-storage syndrome, the accelerator
hypothesis, Gut microbiota and the development of obesity and type 2 diabetes, severe
inflammation and the activation of the immune system, and occupational risk and lifestyle
factors. The findings indicate that obese cases are much more prevalent in individuals with
diabetes, and that obesity, BMI or weight gain plays a significant role in insulin resistance.
There is an increase in the quantity of NEFA, hormones, and pro-inflammatory compounds in
those with obesity because these substances are responsible for insulin resistance. A
dysfunctional beta cell and insulin resistance results in the manifestation of diabetes.
CONCLUSION
Obesity and diabetes are some of the most prevalent illnesses that are on the increase across
the globe. This is despite of the numeral studies that have been done on the possible effective
intervention to prevent and manage the disorders. The current trend shows that both type 1
and type 2 diabetes are prevalent in both children and adults, with noticeable high incidence
among school going children and youths. This overwhelming increase in the incidences of the
disease have attracted the attention of several researches aimed at ascertaining the association
between obesity and diabetes and the corresponding risk factors. As a result, several
theoretical models have been developed on the possible association between diabetes and
obesity. These include Excessive FFAs and Ectopic fat-storage syndrome, the accelerator
hypothesis, Gut microbiota and the development of obesity and type 2 diabetes, severe
inflammation and the activation of the immune system, and occupational risk and lifestyle
factors. The findings indicate that obese cases are much more prevalent in individuals with
diabetes, and that obesity, BMI or weight gain plays a significant role in insulin resistance.
There is an increase in the quantity of NEFA, hormones, and pro-inflammatory compounds in
those with obesity because these substances are responsible for insulin resistance. A
dysfunctional beta cell and insulin resistance results in the manifestation of diabetes.
Running head: Obesity and Diabetes 21
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American Diabetes Association. (2014). Diagnosis and classification of diabetes
mellitus. Diabetes care, 37(Supplement 1), S81-S90.
Atkinson, M. A., Eisenbarth, G. S., & Michels, A. W. (2014). Type 1 diabetes. The
Lancet, 383(9911), 69-82.
Baidal, J. A. W., Locks, L. M., Cheng, E. R., Blake-Lamb, T. L., Perkins, M. E., & Taveras,
E. M. (2016). Risk factors for childhood obesity in the first 1,000 days: a systematic
review. American journal of preventive medicine, 50(6), 761-779.
Bhupathiraju, S. N., & Hu, F. B. (2016). Epidemiology of obesity and diabetes and their
cardiovascular complications. Circulation research, 118(11), 1723-1735.
Blüher, M. (2014). Adipokines–removing road blocks to obesity and diabetes
therapy. Molecular metabolism, 3(3), 230-240.
Boren, J., Taskinen, M. R., Olofsson, S. O., & Levin, M. (2013). Ectopic lipid storage and
insulin resistance: a harmful relationship. Journal of internal medicine, 274(1), 25-40.
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therapy, 7, 587.
American Diabetes Association. (2013). Economic costs of diabetes in the US in
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American Diabetes Association. (2014). Diagnosis and classification of diabetes
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Atkinson, M. A., Eisenbarth, G. S., & Michels, A. W. (2014). Type 1 diabetes. The
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Baidal, J. A. W., Locks, L. M., Cheng, E. R., Blake-Lamb, T. L., Perkins, M. E., & Taveras,
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review. American journal of preventive medicine, 50(6), 761-779.
Bhupathiraju, S. N., & Hu, F. B. (2016). Epidemiology of obesity and diabetes and their
cardiovascular complications. Circulation research, 118(11), 1723-1735.
Blüher, M. (2014). Adipokines–removing road blocks to obesity and diabetes
therapy. Molecular metabolism, 3(3), 230-240.
Boren, J., Taskinen, M. R., Olofsson, S. O., & Levin, M. (2013). Ectopic lipid storage and
insulin resistance: a harmful relationship. Journal of internal medicine, 274(1), 25-40.
Running head: Obesity and Diabetes 22
Byrne, C. D., & Targher, G. (2014). Ectopic fat, insulin resistance, and nonalcoholic fatty
liver disease: implications for cardiovascular disease. Arteriosclerosis, thrombosis,
and vascular biology, ATVBAHA-114.
Choe, S. S., Huh, J. Y., Hwang, I. J., Kim, J. I., & Kim, J. B. (2016). Adipose tissue
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Ganz, M. L., Wintfeld, N., Li, Q., Alas, V., Langer, J., & Hammer, M. (2014). The
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Naseer, M., Bibi, F., H Alqahtani, M., G Chaudhary, A., I Azhar, E., A Kamal, M., & Yasir,
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Running head: Obesity and Diabetes 23
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Health Science, 2(1), 21-38.
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176-179.
McGown, C., Birerdinc, A., & Younossi, Z. M. (2014). Adipose tissue as an endocrine
organ. Clinics in liver disease, 18(1), 41-58.
Running head: Obesity and Diabetes 24
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78.
Menke, A., Casagrande, S., Geiss, L., & Cowie, C. C. (2015). Prevalence of and trends in
diabetes among adults in the United States, 1988-2012. Jama, 314(10), 1021-1029.
Mikkelsen, K. H., Frost, M., Bahl, M. I., Licht, T. R., Jensen, U. S., Rosenberg, J., ... &
Vilsbøll, T. (2015). Effect of antibiotics on gut microbiota, gut hormones and glucose
metabolism. PloS one, 10(11), e0142352.
Minges, K. E., Whittemore, R., & Grey, M. (2013). Overweight and obesity in youth with
type 1 diabetes. Annual review of nursing research, 31, 47.
Mozaffarian D, Benjamin EJ, Go AS, et al. (2015). Heart disease and stroke statistics--2015
update: A report from the American heart association. Circulation. pp131:e29–322.
Retrieved from
https://www.ahajournals.org/doi/abs/10.1161/CIR.0000000000000152?
url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub
%3Dpubmed
Nakamura, K., Fuster, J. J., & Walsh, K. (2014). Adipokines: a link between obesity and
cardiovascular disease. Journal of cardiology, 63(4), 250-259.
Pajunen, P., Rissanen, H., Laaksonen, M. A., Heliövaara, M., Reunanen, A., & Knekt, P.
Running head: Obesity and Diabetes 25
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Running head: Obesity and Diabetes 26
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A. (2014). Diabetes risk among overweight and obese metabolically healthy young
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... & Brams Investigators. (2015). Sagittal abdominal diameter as a surrogate marker
of insulin resistance in an admixtured population—Brazilian Metabolic Syndrome
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Running head: Obesity and Diabetes 27
Appendix: Matrix Table for Literature Review
Literature Review Matrix Template
Refere
nce
Author/
Date –
(APA
Style)
Theo
retic
al/
Conc
eptu
al
Fram
ewor
k
Stud
y
Obje
ctive
s,
Rese
arch
Ques
tion(s
)/
Hypo
these
s
Stud
y
Pop
ulati
on
Meth
odolo
gy
(Type
of
Study
)/
Interv
entio
n
Desig
n (if
applic
able)
Anal
ysis,
Resu
lts &
Major
Findi
ngs
Stre
ngth
s/
Limit
ation
s
Conclus
ions
Recom
mendati
ons
Implic
ations
for
Futur
e
Resea
rch
Implic
ations
for
Practi
ce
Al-
Goblan,
A. S.,
Al-Alfi,
M. A., &
Khan,
M. Z.
(2014).
Mechan
ism
linking
diabete
s
mellitus
and
obesity.
Diabete
s,
metabol
ic
syndro
me and
obesity:
targets
and
therapy,
7, 587.
Obesi
ty
insuli
n
resist
ance
and
obesi
ty
beta
dysfu
nctio
n are
the
linkin
g
mech
anis
m of
obesi
ty
and
diabe
tes
What
is the
linkin
g
mech
anism
betwe
en
obesit
y and
diabet
es
Syst
emat
ic
Liter
ature
revie
w
Syste
matic
literat
ure
review
Cond
ucted
literat
ure
revie
w on
the
linkin
g
mech
anism
betwe
en
diabe
tes
and
obesit
y and
found
out
that
there
was a
positi
ve
relati
onshi
p
betwe
en
body
weigh
NA There is
a
positive
associati
on
between
obesity
and
diabetes.
Need to
study
new
techniqu
es of
managin
g and
preventin
g
diabetes
in obese
patients
More
studie
s to
be
done
on the
effecti
ve
mana
geme
nt and
preve
ntion
of
diabet
es
and
obesit
y
based
on the
finding
s
Diabeti
c and
obese
people
should
be
made
knowle
dgeabl
e on
the
relatio
nship
betwe
en
lifestyl
e
behavi
or and
their
conditi
on
Appendix: Matrix Table for Literature Review
Literature Review Matrix Template
Refere
nce
Author/
Date –
(APA
Style)
Theo
retic
al/
Conc
eptu
al
Fram
ewor
k
Stud
y
Obje
ctive
s,
Rese
arch
Ques
tion(s
)/
Hypo
these
s
Stud
y
Pop
ulati
on
Meth
odolo
gy
(Type
of
Study
)/
Interv
entio
n
Desig
n (if
applic
able)
Anal
ysis,
Resu
lts &
Major
Findi
ngs
Stre
ngth
s/
Limit
ation
s
Conclus
ions
Recom
mendati
ons
Implic
ations
for
Futur
e
Resea
rch
Implic
ations
for
Practi
ce
Al-
Goblan,
A. S.,
Al-Alfi,
M. A., &
Khan,
M. Z.
(2014).
Mechan
ism
linking
diabete
s
mellitus
and
obesity.
Diabete
s,
metabol
ic
syndro
me and
obesity:
targets
and
therapy,
7, 587.
Obesi
ty
insuli
n
resist
ance
and
obesi
ty
beta
dysfu
nctio
n are
the
linkin
g
mech
anis
m of
obesi
ty
and
diabe
tes
What
is the
linkin
g
mech
anism
betwe
en
obesit
y and
diabet
es
Syst
emat
ic
Liter
ature
revie
w
Syste
matic
literat
ure
review
Cond
ucted
literat
ure
revie
w on
the
linkin
g
mech
anism
betwe
en
diabe
tes
and
obesit
y and
found
out
that
there
was a
positi
ve
relati
onshi
p
betwe
en
body
weigh
NA There is
a
positive
associati
on
between
obesity
and
diabetes.
Need to
study
new
techniqu
es of
managin
g and
preventin
g
diabetes
in obese
patients
More
studie
s to
be
done
on the
effecti
ve
mana
geme
nt and
preve
ntion
of
diabet
es
and
obesit
y
based
on the
finding
s
Diabeti
c and
obese
people
should
be
made
knowle
dgeabl
e on
the
relatio
nship
betwe
en
lifestyl
e
behavi
or and
their
conditi
on
Running head: Obesity and Diabetes 28
t and
insuli
n
resist
ance
which
devel
ops
to
diabe
tes
Saboor
Aftab, S.,
Reddy,
N.,
Smith,
E., &
Barber,
T.
(2014).
Obesity
and
Type 2
Diabetes
Mellitus.
Journal
of
Internal
Medicin
e S, 6.
Curre
nt
intrica
te
associ
ation
betwe
en
T2D
and
obesit
y
What
is the
curren
t
associ
ation
betwe
en
diabet
es and
type 2
diabet
es
Syst
emat
ic
Liter
ature
revie
w
Syste
matic
literat
ure
review
Glucot
oxicity
,
impair
ed fat
metab
olism,
entra
nce of
FFAs
into
the
liver,
viscer
al fat
conte
nt are
all
predic
tors of
diabet
es
throu
gh
insulin
resista
nce
NA Type 2
diabetes
is
associate
d with
impaired
fat
metabolis
m.
Additional
studies on
the
specific
mechanis
ms in
which
lipotoxicit
y leads to
the type 2
diabetes
The
finding
s will
trigger
the
design
of
strateg
ies to
preven
t and
manag
e T2D
The
lifestyl
e of
diabeti
c and
obese
patient
s
should
be
regulat
ed as
an
effectiv
e
interve
ntion
Naseer,
M., Bibi,
F., H
Alqahtan
i, M., G
Chaudha
ry, A., I
Azhar,
E., A
Kamal,
M., &
Yasir,
M.
The
functi
on of
gut
micro
biota
in T2D
and
obesit
y
Does
the
gut
micro
biota
have a
role in
obesit
y and
T2D?
Syst
emat
ic
Liter
ature
revie
w
Syste
matic
literat
ure
review
Studie
s have
show
n the
involv
ement
of gut
micrio
biota
in the
devel
opme
NA Existing
research
has
pointed
out that
gut
microbiot
a has a
significant
role in
obesity
and risk
factors
Furthe
r
studies
should
be
objecti
ve on
describ
ing the
compa
rative
contrib
Prebio
tics
should
be
utilized
in the
preven
tion of
disorde
rs
related
to
weight
t and
insuli
n
resist
ance
which
devel
ops
to
diabe
tes
Saboor
Aftab, S.,
Reddy,
N.,
Smith,
E., &
Barber,
T.
(2014).
Obesity
and
Type 2
Diabetes
Mellitus.
Journal
of
Internal
Medicin
e S, 6.
Curre
nt
intrica
te
associ
ation
betwe
en
T2D
and
obesit
y
What
is the
curren
t
associ
ation
betwe
en
diabet
es and
type 2
diabet
es
Syst
emat
ic
Liter
ature
revie
w
Syste
matic
literat
ure
review
Glucot
oxicity
,
impair
ed fat
metab
olism,
entra
nce of
FFAs
into
the
liver,
viscer
al fat
conte
nt are
all
predic
tors of
diabet
es
throu
gh
insulin
resista
nce
NA Type 2
diabetes
is
associate
d with
impaired
fat
metabolis
m.
Additional
studies on
the
specific
mechanis
ms in
which
lipotoxicit
y leads to
the type 2
diabetes
The
finding
s will
trigger
the
design
of
strateg
ies to
preven
t and
manag
e T2D
The
lifestyl
e of
diabeti
c and
obese
patient
s
should
be
regulat
ed as
an
effectiv
e
interve
ntion
Naseer,
M., Bibi,
F., H
Alqahtan
i, M., G
Chaudha
ry, A., I
Azhar,
E., A
Kamal,
M., &
Yasir,
M.
The
functi
on of
gut
micro
biota
in T2D
and
obesit
y
Does
the
gut
micro
biota
have a
role in
obesit
y and
T2D?
Syst
emat
ic
Liter
ature
revie
w
Syste
matic
literat
ure
review
Studie
s have
show
n the
involv
ement
of gut
micrio
biota
in the
devel
opme
NA Existing
research
has
pointed
out that
gut
microbiot
a has a
significant
role in
obesity
and risk
factors
Furthe
r
studies
should
be
objecti
ve on
describ
ing the
compa
rative
contrib
Prebio
tics
should
be
utilized
in the
preven
tion of
disorde
rs
related
to
weight
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Running head: Obesity and Diabetes 29
(2014).
Role of
gut
microbio
ta in
obesity,
type 2
diabetes
and
Alzheim
er’s
disease.
CNS &
Neurolo
gical
Disorder
s-Drug
Targets
(Formerl
y
Current
Drug
Targets-
CNS &
Neurolo
gical
Disorder
s), 13(2),
305-311.
nt of
obesit
y and
the
metab
olism
of the
host
for T2D utions
of the
comm
unicati
on
pathw
ays of
the gut
microb
iota
with
the
central
nervou
s
system
to
explor
e the
likeliho
od of
associa
tion
betwe
en the
microb
iota
and
the
develo
pment
of
Alzhei
mer’s
diseas
e
gain as
a
supple
ment
diet
that
triggers
the
growth
of
some
microb
es to
enhanc
e
metab
olism
Devaraj,
S.,
Hemaraj
ata, P., &
Versalov
ic, J.
(2013).
The
human
gut
microbio
me and
body
metaboli
The
huma
n
micro
biome
gut
can
lead
to
elevat
ed
preval
ence
of
What
is the
role of
the
huma
n
micro
biome
gut in
the
increa
se of
obesit
y and
Syst
emat
ic
Liter
ature
revie
w
Syste
matic
literat
ure
review
The
gut
micro
biota
influe
nces
the
intake
of
nutrie
nts,
energ
y
consol
NA Advanced
research
in human
studies
will
provide
in-depth
understan
ding of
the
function
of gut
mibrobio
me in the
Furthe
r
studies
should
be
conduc
ted to
provid
e
deeper
unders
tandin
g of
The
microb
es in
the gut
microbi
ota
should
be
utilized
in the
preven
tion
and
treatm
(2014).
Role of
gut
microbio
ta in
obesity,
type 2
diabetes
and
Alzheim
er’s
disease.
CNS &
Neurolo
gical
Disorder
s-Drug
Targets
(Formerl
y
Current
Drug
Targets-
CNS &
Neurolo
gical
Disorder
s), 13(2),
305-311.
nt of
obesit
y and
the
metab
olism
of the
host
for T2D utions
of the
comm
unicati
on
pathw
ays of
the gut
microb
iota
with
the
central
nervou
s
system
to
explor
e the
likeliho
od of
associa
tion
betwe
en the
microb
iota
and
the
develo
pment
of
Alzhei
mer’s
diseas
e
gain as
a
supple
ment
diet
that
triggers
the
growth
of
some
microb
es to
enhanc
e
metab
olism
Devaraj,
S.,
Hemaraj
ata, P., &
Versalov
ic, J.
(2013).
The
human
gut
microbio
me and
body
metaboli
The
huma
n
micro
biome
gut
can
lead
to
elevat
ed
preval
ence
of
What
is the
role of
the
huma
n
micro
biome
gut in
the
increa
se of
obesit
y and
Syst
emat
ic
Liter
ature
revie
w
Syste
matic
literat
ure
review
The
gut
micro
biota
influe
nces
the
intake
of
nutrie
nts,
energ
y
consol
NA Advanced
research
in human
studies
will
provide
in-depth
understan
ding of
the
function
of gut
mibrobio
me in the
Furthe
r
studies
should
be
conduc
ted to
provid
e
deeper
unders
tandin
g of
The
microb
es in
the gut
microbi
ota
should
be
utilized
in the
preven
tion
and
treatm
Running head: Obesity and Diabetes 30
sm:
implicati
ons for
obesity
and
diabetes
. Clinical
chemistr
y,
clinchem
-2012.
obesit
y and
diabet
es
diabet
es
preval
ence
idatio
n, and
severa
l
metab
olism
pathw
ays of
the
host
cardiovas
cular
disorders
the
role of
gut
microb
iota in
human
metab
olism
ent of
metab
olic
disorde
rs
Esser,
N.,
Legrand-
Poels, S.,
Piette, J.,
Scheen,
A. J., &
Paquot,
N.
(2014).
Inflamm
ation as
a
link
between
obesity,
metaboli
c
syndrom
e and
type 2
diabetes
. Diabet
es
research
and
clinical
practice,
105(2),
141-150.
Inflam
matio
n is
the
conne
cting
mech
anism
betwe
en
T2D,
obesit
y and
meta
bolic
syndr
ome
How is
inflam
matio
n the
linking
mecha
nism
betwe
en
obesit
y, T2D
and
metab
olic
syndr
ome?
Syst
emat
ic
Liter
ature
revie
w
Syste
matic
literat
ure
review
Low
grade
inflam
matio
n and
the
stimul
ation
of the
immu
ne
syste
m are
engag
ed in
the
devel
opme
nt of
insulin
resista
nce
which
is
obesit
y, and
T2D
relate
d
NA The
immune
system
has a role
in insulin
resistance
and T2D.
Type 2
diabetes
can be
treated
and
prevente
d using
anti-
inflammat
ory
therapies.
More
studies
should
be
conduc
ted to
ascerta
in the
underl
ying
mecha
nisms
of the
associa
tion
betwe
en the
immun
e
system
and
the
manife
station
of
insulin
resista
nce
Anti-
inflam
matory
therapi
es can
be
used in
the
treatm
ent and
preven
tion of
T2D
since it
is an
inflam
matory
disorde
r
sm:
implicati
ons for
obesity
and
diabetes
. Clinical
chemistr
y,
clinchem
-2012.
obesit
y and
diabet
es
diabet
es
preval
ence
idatio
n, and
severa
l
metab
olism
pathw
ays of
the
host
cardiovas
cular
disorders
the
role of
gut
microb
iota in
human
metab
olism
ent of
metab
olic
disorde
rs
Esser,
N.,
Legrand-
Poels, S.,
Piette, J.,
Scheen,
A. J., &
Paquot,
N.
(2014).
Inflamm
ation as
a
link
between
obesity,
metaboli
c
syndrom
e and
type 2
diabetes
. Diabet
es
research
and
clinical
practice,
105(2),
141-150.
Inflam
matio
n is
the
conne
cting
mech
anism
betwe
en
T2D,
obesit
y and
meta
bolic
syndr
ome
How is
inflam
matio
n the
linking
mecha
nism
betwe
en
obesit
y, T2D
and
metab
olic
syndr
ome?
Syst
emat
ic
Liter
ature
revie
w
Syste
matic
literat
ure
review
Low
grade
inflam
matio
n and
the
stimul
ation
of the
immu
ne
syste
m are
engag
ed in
the
devel
opme
nt of
insulin
resista
nce
which
is
obesit
y, and
T2D
relate
d
NA The
immune
system
has a role
in insulin
resistance
and T2D.
Type 2
diabetes
can be
treated
and
prevente
d using
anti-
inflammat
ory
therapies.
More
studies
should
be
conduc
ted to
ascerta
in the
underl
ying
mecha
nisms
of the
associa
tion
betwe
en the
immun
e
system
and
the
manife
station
of
insulin
resista
nce
Anti-
inflam
matory
therapi
es can
be
used in
the
treatm
ent and
preven
tion of
T2D
since it
is an
inflam
matory
disorde
r
1 out of 30
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