The Relationship Between Obesity and Type 2 Diabetes Mellitus

This report discusses the relationship between obesity and type 2 diabetes mellitus, focusing on the interrelation between dysfunction of pancreatic β-cell and insulin resistance with obesity. It explores the mechanisms through which obesity promotes type 2 diabetes and the genetic factors linking obesity to diabetes. Recommendations for managing body weight and preventing type 2 diabetes are also provided.

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THE RELATIONSHIP BETWEEN OBESITY AND TYPE 2 DIABETES MELLITUS
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Obesity and type 2 diabetes 2
Abstract
Diabetes and insulin resistance are strongly correlated to body mass index. For individuals who
are obese, the quantity of glycerol, proinflammatory markers, nonesterified fatty acids, and
cytokines among other elements that play a role in the advancement of resistance to insulin is
augmented. Impairment of the pancreatic Beta islet cells and thus causing improper control of
the blood sugar form the foundation of diabetes pathogenesis. Type 2 diabetes mellitus
progression is accelerated when insulin resistance accompanies impairment of the pancreatic
Beta islet cells. It is therefore undoubtable that high body mass index and progressive weight
gain are key contributors to the rising occurrence of type 2 diabetes. In this report, therefore,
comprehensive inscription of the interrelation between dysfunction of pancreatic β-cell and
insulin resistance with obesity is made.

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1.0 Introduction
Diabetes mellitus is a long term disorder with the potential of altering the metabolism of fats,
proteins and carbohydrates. It is primarily caused by low secretion of insulin due to either
marked or advanced incapability of the pancreatic β-Langerhans islet cells to yield insulin. It can
also be caused by defective uptake of insulin in the outlying flesh. There are two broad
classifications of diabetes which are; type 1 diabetes mellitus and type 2 diabetes mellitus.
The etiology and pathophysiology of type 2 diabetes are relatively different in comparison to that
of type 1 diabetes. Type 2 diabetes is the utmost established and is commonly characterized by
either production of insulin in low amounts from the pancreatic Beta cells or resistance of insulin
in the peripheral tissue (Sheehan & Ulchaker, 2011). When resistance to insulin occurs, the level
of plasmic fatty acids elevates subsequently lowering transport of glucose into the muscle cells
and elevatin itemization of fats. Consequently, hepatic glucose production raises. Development
of type II diabetes requires the simultaneous occurrence of pancreatic Beta-cell dysfunction and
insulin resistance must prevail. Being obese emanates from some kind of insulin resistance and
thus plays a significant role in the progression of type 2 diabetes.
In Australia, type 2 diabetes is a menace that is negatively impacting the lives of people. The
disease was traditionally associated with the elderly people but the trend is currently changing
(Ahmad, 2013). Recent reports indicate that with the ever-changing lifestyle, the incidence of
type 2 diabetes is increasing even to the younger generation. This report will therefore
comprehensively discuss how obesity plays part in promoting type 2 diabetes among individuals
aged 30-50 years. It will commence with a discussion of obesity-related factors that accelerate
the threat of acquiring type 2 diabetes. This section will adopt relevant literature and bring into
the limelight insulin resistance mechanisms associated to obesity, progressive β-cell dysfunction

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mechanisms in obese persons, genetic aspects associating obesity to diabetes and the possibility
of shared pathogenesis between obesity and type 2 diabetes mellitus. It will conclude with
recommendations that could be implemented to curb the menace in Australia.
2.1 Means through which obesity promotes type 2 diabetes among people aged 30-50 years.
2.1.1 Insulin resistance mechanisms associated with obesity
Type 2 diabetes is not only influenced by obesity through the degree of resistance to insulin but
also by the body part where fat amasses. Accumulation of fat in the upper body such as visceral
adiposity, which manifests itself through increased weight to hip ratio or abdominal girth is
directly concomitant to cardiovascular disease, metabolic disorder and more so, type 2 diabetes.
Other than differences in the distribution of the body fat, upcoming evidence put it forward that
glucose homeostasis is affected differently by adipose tissue of different subtypes which function
distinctly (Chadt, et al., 2018). Adults, including those in the category of 30-50 years, have
variable and limited numbers of brown fat cells. These cells are largely involved in
thermogenesis in addition to having the potential of influencing the expenditure of energy and
susceptibility to obesity.
There are three distinct and key modes of action that have been suggested to interconnect obesity
and insulin resistance and consequently predisposing obese persons to type 2 diabetes. The first
mechanism involves increased production of cytokines or adipokines. They include the retinol
binding protein 4, resistin and the tumor necrosis factor-α. All the aforementioned have been
proved to contribute to lowered levels of adiponectin production as well as raising the resistance
of the body to insulin. The second mechanism centers on the deposition of ectopic fat (Al-
Goblan, et al., 2014). The body parts that are particularly affected by this deposition are the
dysmetabolic sequelae, skeletal muscle and more importantly in the liver. The last mechanism is

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dysfunction of the mitochondria which is evidenced by lowered functioning of the mitochondria
or decreased mitochondrial mass. This mechanism is marked as one of the many significant
defects that links diabetes to obesity. It has two key modes of action which are; compromising
the functionality of theβ-cell, and lowering insulin sensitivity (Ota, 2015).
2.1.2 Progressive β-cell dysfunction mechanisms in obese persons.
Despite their fragility, the β-cells have a significant role in controlling the release of insulin. The
amount, route of administration and nature of stimulus causes changes and fluctuations in the
measure of insulin secreted by the β-cells (Fantuzzi & Braunschweig, 2014). As such the β-cell
play a significant role in ensuring that the stability of blood glucose concentrations is maintained
within the normal physiological range. In obese people, however, the modulation of the beta cell
function, as well as insulin sensitivity, decreases significantly.
In ordinary fit individuals, there exists an uninterrupted response liaison between the insulin-
sensitive tissues and the β-cells. Whenever there is a demand for the supply of glucose in the
muscles, liver and tissues, there is a consequent supply of insulin by the β-cells (Barnett &
Kumar, 2005). If stability is required in the glucose levels, insulin sensitivity changes must be in
line with a matching level of change in the circulating insulin. If however this process fails to
take place and there is a mismatch, glucose levels are deregulated and subsequently leading to
advancement of prediabetes. If the beta cells are in fine fettle in the body, insulin resistance is
countered by an adaptive response which in turn facilitates maintenance of normal glucose levels
(Draznin & Rizza, 2013). Contrary, impairment of the pancreatic β-cells may cause the
development of abnormal glucose fasting or abnormal glucose tolerance. Consequently, type 2
diabetes mellitus begins developing.

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Continuous deterioration in the functionality of the pancreatic β-cells gradually instigates the
development of type 2 diabetes mellitus. Literature states that low secretion of insulin emanating
from dysfunction of the beta cells causes elevation of postprandial blood glucose as well as
fasting blood glucose (Litwack, 2014). As a result, the incomplete or absent reticence of glucose
formation in the liver will cause lowered efficiency of the muscle and hepatic uptake of glucose.
As blood glucose further increases, the severity of type 2 diabetes will prevail manifesting
through effects of glucotoxicity on the pancreatic β-cells, as well as the negative implications on
the peripheral tissue sensitivity as well as uptake of insulin.
2.1.3 Genetic factors linking obesity to diabetes.
Forty genes allied with type 2 diabetes and linked to obesity have been brought into the limelight
by candidate gene approaches as well as Genome Wide Association Scans (GWAS) (Al-Goblan,
et al., 2014). Although a wide range of diabetes type 2 genes are related to pancreatic β-cells
dysfunction, few of them are connected to pathways related to the resistance of insulin but
independent of obesity. Additionally, it has been observed that many variants of obesity genes
are involved in pathways affecting the homeostasis of energy (Burtis, et al., 2012). Albeit
identification of numerous obesity and diabetes related genes has been made, the known genes
are projected to forecast 5%of obesity and 15% of diabetes type 2. Even though it is undoubtable
that more genes revealing more significant interconnections between obesity and type 2 diabetes
mellitus will be revealed, the aforementioned low projecting power reflects the significance of
environmental factors, less frequent genetic variants with stronger implications, or gene-gene,
gene-environment as well as other epigenetic variations.
2.1.4 Does obesity and type 2 diabetes mellitus have shared pathogenesis?

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The interconnection between obesity and type 2 diabetes mellitus is largely attributed to two
mechanisms; the pancreatic Beta-cell failure and obesity instigated resistance to insulin. As such,
the two mechanisms brings forth the possibility of the two disorders sharing a common
underlying defect. With reference to the unified field theory, questions are raised whether de-
compensation of pancreatic beta cells is accelerated by metabolic impairment as well as
continuous weight gain (DeFronzo, et al., 2015).
One key link is sustained exposure of the cells to nutrient concentrations high above the energy
requirements. Excess nutrients are known to cause cellular implications of a deleterious nature
such as stress on the endoplasmic reticulum, impaired inflammatory signaling, production of
reactive oxygen species at an abnormally higher quantity, and accumulation of fatty acyl
intermediates (Draznin & Rizza, 2013). All the aforementioned responses do not display mutual
exclusivity and thus a cascade of damage may be caused by the induction of one response which
subsequently triggers another. As a result, cellular injuries associated with obesity recruit and
activate a variety of immune cells among them macrophages that trigger and fuel inflammation
of tissues. Jointly, all these responses contribute in the advancement of insulin resistance in the
skeletal muscles, the liver, and the adipose tissue.
In individuals between 30-50 years who have a higher susceptibility by exposing themselves to
obesity-causing factors, metabolic impairment induced by obesity can facilitate dysfunction of
pancreatic beta cells on one hand and insulin resistance on the other. The problem of excess
nutrients may be worsened by lowered secretion of insulin by escalating the concentrations of
free fatty acids and glucose circulating in the blood (Al-Goblan, et al., 2014). It is by this mode
of action that a vicious cycle arises and through which excess nutrients brought about by obesity
prompts inflammatory comebacks that bring about insulin resistance. Consequently, a higher

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demand is placed on the beta cells and as the functionality of the beta cells lowers, an increase in
the cellular toll taken by the nutrient surplus is realized.
2.2 recommendations
Having ascertained that indeed obesity promotes type 2 diabetes among individuals aged 30-50
years, the following recommendation could aid curbing the interconnection between the two
chronic illnesses. This could be basically achieved through maintenance of the right body mass
index as discussed below.
2.2.1 Body weight management through a change of behavior and use of medication
The notable rise in prevalence and incidence of obesity among individuals between 30-50 years
old in Australia has been associated with alterations in dietary composition or intake of calorie.
Prevention measures have focused on the intervention of lifestyles to ameliorate or reverse the
caloric imbalance (Rippe & Angelopoulos, 2012). Designing 6-12 months long programs to be
implemented at either individual or group level can play a significant role by offering to counsel
on means of modifying behavior. For a lifestyle intervention program to be successful, the key
activities to be indulged in include but not limited to being physically active, self-monitoring of
body mass index, and having a good dietary plan (Bagchi & Nair, 2012).
In addition to the aforementioned behavioral interventions, medications which have been in use
for decades to aid in weight loss could be a perfect choice for Australians incorporated in the
report. Physiological insights have steered the development of medications with the most recent
advancements focusing on the central nervous system to control metabolism and appetite.
2.2.2 Undergoing bariatric surgery to manage body weight.

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Based on data emanating from nonrandomized studies, it has emerged that bariatric surgery is
becoming more and more popular due to the health benefits it has. Some of the key benefits are
sustained substantial loss of weight and rectification of comorbidities such as dyslipidemia,
hypertension and more importantly, type 2 diabetes (Faintuch & Faintuch, 2014). This method,
therefore, turns out to be a good choice for obese Australians to lose weight and consequently
reduce the risk of acquiring obesity-induced diabetes or increasing its severity.
3.0 Conclusion.
Conclusively, this report commenced with an overview of the research question bringing into the
limelight substantial knowledge of type 2 diabetes. Next on, a comprehensive discussion of the
means through which obesity promotes type 2 diabetes among Australians aged 30-50 years has
been brought forth. The modes of action interrelating the two chronic illnesses that have been
discussed are insulin resistance mechanisms associated to obesity, progressive β-cell dysfunction
mechanisms in obese persons, genetic factors associating obesity to diabetes and the possibility
of joint pathogenesis between obesity and type 2 diabetes mellitus. All the aforementioned
discussions have proved that indeed obesity is directly involved in raising the risk of acquiring
type two diabetes or increasing its severity. The report has finalized by laying out
recommendations that could be implemented in Australia to curb obesity. Consequently,
implementation of these recommendations will go a long way into lowering incidences of type 2
diabetes mellitus.

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4.0 References
Ahmad, S. I., 2013. Diabetes: An Old Disease, a New Insight. Illustrated ed. s.l.:Springer
Science & Business Media.
Al-Goblan, A. S., Al-Alifi, M. A. & Khan, M. Z., 2014. Mechanism linking diabetes mellitus
and obesity. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy.
Bagchi, D. & Nair, S., 2012. Nutritional and Therapeutic Interventions for Diabetes and
Metabolic Syndrome. 2 ed. s.l.:Academic Press.
Barnett, A. H. & Kumar, S., 2005. Obesity and Diabetes. Reprint ed. s.l.:John Wiley & Sons.
Burtis, C. A., Ashwood, E. & Bruns, D., 2012. Tietz Textbook of Clinical Chemistry and
Molecular Diagnostics - E-Book. 5 ed. s.l.:Elsevier Health Sciences.
Chadt, A., Scherneck, S., Joost, H.-G. & Al-Hasani, H., 2018. Molecular links between Obesity
and Diabetes: “Diabesity”. Endotext, 18 Jan.
DeFronzo, R. A., Ferrannini, E., Zimmet, P. & Alberti, G., 2015. International Textbook of
Diabetes Mellitus, 2 Volume Set, Volume 1. 4, illustrated, reprint ed. s.l.:John Wiley & Sons.
Draznin, B. & Rizza, R., 2013. Clinical Research in Diabetes and Obesity, Volume 2: Diabetes
and Obesity. Illustrated ed. s.l.:Springer Science & Business Media.
Faintuch, J. & Faintuch, S., 2014. Obesity and Diabetes: New Surgical and Nonsurgical
Approaches. Illustrated ed. s.l.:Springer publishers.
Fantuzzi, G. & Braunschweig, C., 2014. Adipose Tissue and Adipokines in Health and Disease.
2, illustrated, revised ed. s.l.:Springer Science & Business.

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Litwack, G., 2014. The Pancreatic Beta Cell. illustrated ed. s.l.:Elsevier Science.
Ota, T., 2015. Obesity-induced inflammation and insulin resistance. Illustrated ed. s.l.:Frontiers
Media SA.
Rippe, J. M. & Angelopoulos, T., 2012. Obesity: Prevention and Treatment. illustrated ed.
s.l.:CRC Press.
Sheehan, J. & Ulchaker, M. M., 2011. Obesity and Type 2 Diabetes Mellitus. illustrated, reprint
ed. s.l.:Oxford University Press.