Understanding Type 2 Diabetes: Biological Aspects, Progression, and Potential Outcomes
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This document provides an in-depth understanding of type 2 diabetes, including its biological and physiological aspects, disease progression, potential outcomes, and treatment options. It explores the pathways affected by the disease and discusses the impact of type 2 diabetes on various body systems. The document also highlights the potential complications and risks associated with this condition.
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Running Head: DIABETES
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DIABETES
1
Table of Contents
Introduction................................................................................................................................2
Biological and physiological aspects......................................................................................2
Chemical treatment.................................................................................................................2
Pathways affected by the disease...........................................................................................3
Disease progression................................................................................................................3
Beta Cell Failure.................................................................................................................4
Potential outcomes..................................................................................................................4
Conclusion..................................................................................................................................5
Reference....................................................................................................................................6
1
Table of Contents
Introduction................................................................................................................................2
Biological and physiological aspects......................................................................................2
Chemical treatment.................................................................................................................2
Pathways affected by the disease...........................................................................................3
Disease progression................................................................................................................3
Beta Cell Failure.................................................................................................................4
Potential outcomes..................................................................................................................4
Conclusion..................................................................................................................................5
Reference....................................................................................................................................6
DIABETES
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Introduction
Type-2 diabetes is the health condition in which the body cells are not able to use
blood sugar (glucose) proficiently for energy production. This occurs when the body cells
developed unresponsive to insulin and the levels of blood sugar increases gradually. There
are two different kinds of diabetes mellitus, type one and type two. In type two, the pancreas
able to create insulin, on the other hand, the cells is unable to use it very proficiently
(Chatterjee, Khunti, & Davies, 2017). In these particular report biological and physiological
aspects, natural progression, and potential outcomes of diabetes type 2 will be discussed.
Biological and physiological aspects
In diabetes category 2, the human body either creates insufficient quantities of insulin
to encounter the requirements of the body or the resistance of insulin has advanced. The
resistance of insulin refers to when the body cells like the muscle, liver cells and fat cells are
unsuccessful to react to insulin hormone, even when amounts are great. In the fat cells,
triglycerides are cracked down to create free fatty acids for the production of energy; muscle-
derived cells and liver cells are without a source of energy be unsuccessful to form up
glycogen stocks. This also results in a complete rise in the glucose amount in the blood.
Glycogen stocks become evidently decreased and there is insufficient glucose accessible for
discharge when it might be required (Zaccardi, Webb, Yates, & Davies, 2016).
Chemical treatment
Metformin (Glucophage, Glumetza, others); generally, metformin is the principal
medication recommended for category 2 diabetes. It functions by dropping glucose creation
2
Introduction
Type-2 diabetes is the health condition in which the body cells are not able to use
blood sugar (glucose) proficiently for energy production. This occurs when the body cells
developed unresponsive to insulin and the levels of blood sugar increases gradually. There
are two different kinds of diabetes mellitus, type one and type two. In type two, the pancreas
able to create insulin, on the other hand, the cells is unable to use it very proficiently
(Chatterjee, Khunti, & Davies, 2017). In these particular report biological and physiological
aspects, natural progression, and potential outcomes of diabetes type 2 will be discussed.
Biological and physiological aspects
In diabetes category 2, the human body either creates insufficient quantities of insulin
to encounter the requirements of the body or the resistance of insulin has advanced. The
resistance of insulin refers to when the body cells like the muscle, liver cells and fat cells are
unsuccessful to react to insulin hormone, even when amounts are great. In the fat cells,
triglycerides are cracked down to create free fatty acids for the production of energy; muscle-
derived cells and liver cells are without a source of energy be unsuccessful to form up
glycogen stocks. This also results in a complete rise in the glucose amount in the blood.
Glycogen stocks become evidently decreased and there is insufficient glucose accessible for
discharge when it might be required (Zaccardi, Webb, Yates, & Davies, 2016).
Chemical treatment
Metformin (Glucophage, Glumetza, others); generally, metformin is the principal
medication recommended for category 2 diabetes. It functions by dropping glucose creation
DIABETES
3
in the human liver and enhancing the insulin sensitivity of the body in order to use insulin
more efficiently (Forslund et al., 2015).
Sulfonylureas; These medicines assist the body discharge more insulin. Illustrations include
glyburide, glimepiride, and glipizide. Probable negative effects comprise decreased blood
sugar and increased weight (Yu, Azoulay, Yin, Filion, & Suissa, 2018).
Meglitinides; these medicines like repaglinide and nateglinide act like sulfonylureas by
triggering the pancreas to discharge additional insulin, nonetheless, they are quicker
performing, and the period of their outcome in the human body is lesser. These medicines
also have the risk of producing low levels of blood sugar and increases in weight.
Thiazolidinedione; similar to metformin, these medicines counting rosiglitazone and
pioglitazone cause the tissues of the body further sensitive to insulin (Dawed, et al., 2016).
DPP-4 inhibitors; these drugs such as sitagliptin, linagliptin, and saxagliptin assist the body to
decrease blood sugar amount, however, tend to exert a very diffident effect.
SGLT2 inhibitors; these medications inhibit the kidneys from sugar reabsorptions into the
bloodstream. In its place, the sugar is defecated in the urine (Scheen, 2015).
Pathways affected by the disease
There are many different body pathways that are affected by this health issues some
of them are KEGG adipocytokine signaling pathways, biocarta prara pathway, Reactome
P12K carcade, KEGG insulin signaling pathway, ST stat 3 pathway, and Biocarta il 6
pathway (Allin, Nielsen, & Pedersen, 2015).
3
in the human liver and enhancing the insulin sensitivity of the body in order to use insulin
more efficiently (Forslund et al., 2015).
Sulfonylureas; These medicines assist the body discharge more insulin. Illustrations include
glyburide, glimepiride, and glipizide. Probable negative effects comprise decreased blood
sugar and increased weight (Yu, Azoulay, Yin, Filion, & Suissa, 2018).
Meglitinides; these medicines like repaglinide and nateglinide act like sulfonylureas by
triggering the pancreas to discharge additional insulin, nonetheless, they are quicker
performing, and the period of their outcome in the human body is lesser. These medicines
also have the risk of producing low levels of blood sugar and increases in weight.
Thiazolidinedione; similar to metformin, these medicines counting rosiglitazone and
pioglitazone cause the tissues of the body further sensitive to insulin (Dawed, et al., 2016).
DPP-4 inhibitors; these drugs such as sitagliptin, linagliptin, and saxagliptin assist the body to
decrease blood sugar amount, however, tend to exert a very diffident effect.
SGLT2 inhibitors; these medications inhibit the kidneys from sugar reabsorptions into the
bloodstream. In its place, the sugar is defecated in the urine (Scheen, 2015).
Pathways affected by the disease
There are many different body pathways that are affected by this health issues some
of them are KEGG adipocytokine signaling pathways, biocarta prara pathway, Reactome
P12K carcade, KEGG insulin signaling pathway, ST stat 3 pathway, and Biocarta il 6
pathway (Allin, Nielsen, & Pedersen, 2015).
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DIABETES
4
Disease progression
Beta cell performance deterioration seems to be slow during the growth and
progression of diabetes type 2 (Violi, Targher, Vestri, Carnevale, Averna, Farcomeni, Lenzi,
Angelico, Cipollone, and Pastori, 2017). It is found that the liberal reduction in secretion of
insulin by beta cell, principally the first-phase insulin discharge that happens acutely
afterward an upsurge in the glycemia, is probably the most serious serviceable beta cell fault
in the growth of diabetes type 2. The investigation indicates that the reduction in suitable
insulin excretion can instigate as quickly as twelve years earlier the patient is identified with
diabetes type 2.
Beta Cell Failure
Typically, beta cells work to compensate for elevated blood glucose levels by
increasing insulin secretion. Over a period, insulin resistance upsurges, and though a lot of
insulin is created, it is not adequate to control blood glucose intensities (Dooley, et al., 2016).
Finally, the beta cells may instigate to misplace their receptiveness to raised glucose
intensities. “Chronic hyperglycemia reduces insulin-secreting granules from the β cells,
decreasing the levels of insulin obtainable to be discharged in reaction to novel glucose
inducements,” investigators describe (Violi, et al., 2017). In adding, it is supposed that great
levels of flowing fatty acids may also harmfully influence beta cell task. “Persistent upsurges
in free fatty acid intensities unfavorably affect the alteration of proinsulin to the insulin and
ultimately disturb insulin excretion. Fatty penetration of pancreatic islets might also subsidize
to dysfunction of the beta cell, and pancreatic fat associates harmfully with the function of the
beta cell (Xin et al., 2016). Swelling, in specific, which is related to extreme weight, is
likewise a supposed culprit in deteriorating function of the beta cell. The particular molecular
4
Disease progression
Beta cell performance deterioration seems to be slow during the growth and
progression of diabetes type 2 (Violi, Targher, Vestri, Carnevale, Averna, Farcomeni, Lenzi,
Angelico, Cipollone, and Pastori, 2017). It is found that the liberal reduction in secretion of
insulin by beta cell, principally the first-phase insulin discharge that happens acutely
afterward an upsurge in the glycemia, is probably the most serious serviceable beta cell fault
in the growth of diabetes type 2. The investigation indicates that the reduction in suitable
insulin excretion can instigate as quickly as twelve years earlier the patient is identified with
diabetes type 2.
Beta Cell Failure
Typically, beta cells work to compensate for elevated blood glucose levels by
increasing insulin secretion. Over a period, insulin resistance upsurges, and though a lot of
insulin is created, it is not adequate to control blood glucose intensities (Dooley, et al., 2016).
Finally, the beta cells may instigate to misplace their receptiveness to raised glucose
intensities. “Chronic hyperglycemia reduces insulin-secreting granules from the β cells,
decreasing the levels of insulin obtainable to be discharged in reaction to novel glucose
inducements,” investigators describe (Violi, et al., 2017). In adding, it is supposed that great
levels of flowing fatty acids may also harmfully influence beta cell task. “Persistent upsurges
in free fatty acid intensities unfavorably affect the alteration of proinsulin to the insulin and
ultimately disturb insulin excretion. Fatty penetration of pancreatic islets might also subsidize
to dysfunction of the beta cell, and pancreatic fat associates harmfully with the function of the
beta cell (Xin et al., 2016). Swelling, in specific, which is related to extreme weight, is
likewise a supposed culprit in deteriorating function of the beta cell. The particular molecular
DIABETES
5
methods underlying how swelling affects the beta function of a cell can be unraveled (Violi,
et al., 2017).
Potential outcomes
The uncontrolled diabetes type leads to impairment to the big blood vessels present in
the heart, mind, and legs. It also causes damage to the minor blood vessels, producing
glitches in the eye bolls, kidneys function, feet, and the nerves. Other regions of the human
body can likewise be exaggerated by diabetes, counting the digestive scheme, the skin,
sensual organs, teeth and the gums, and the resistant system. Types 2 Diabetes also upsurge
the probabilities of heart connected issues because of the high levels of cholesterol. People
with category 2 diabetes transmit a fifteen percent augmented threat of early death associated
with healthy individuals (Marso, et al., 2016).
Conclusion
The type 2 diabetes is the health issue that causes the blood cells unable to use the sugar
present in the blood effectively. In these health conditions, there is a lack of insulin to fulfill the
requirements of the body and the insulin resistance is also increased. Some of the medicines can
be beneficial in are metformin, Sulfonylureas, Meglitinides, Thiazolidinedione, DPP-4
inhibitors, and SGLT2 inhibitors. The pathways affected by this health condition include
KEGG adipocytokine signaling pathways, biocarta prara pathway, and ST stat 3 pathways.
The progression starts with the functional deterioration of beta cells and leads to failure. And
inflammations some of the potential outcomes in that occurs are impairments to blood
vessels, legs, heart, mind, issues in kidney function, gums, teeth, skin sexual parts, and in
severe cases even cause death.
5
methods underlying how swelling affects the beta function of a cell can be unraveled (Violi,
et al., 2017).
Potential outcomes
The uncontrolled diabetes type leads to impairment to the big blood vessels present in
the heart, mind, and legs. It also causes damage to the minor blood vessels, producing
glitches in the eye bolls, kidneys function, feet, and the nerves. Other regions of the human
body can likewise be exaggerated by diabetes, counting the digestive scheme, the skin,
sensual organs, teeth and the gums, and the resistant system. Types 2 Diabetes also upsurge
the probabilities of heart connected issues because of the high levels of cholesterol. People
with category 2 diabetes transmit a fifteen percent augmented threat of early death associated
with healthy individuals (Marso, et al., 2016).
Conclusion
The type 2 diabetes is the health issue that causes the blood cells unable to use the sugar
present in the blood effectively. In these health conditions, there is a lack of insulin to fulfill the
requirements of the body and the insulin resistance is also increased. Some of the medicines can
be beneficial in are metformin, Sulfonylureas, Meglitinides, Thiazolidinedione, DPP-4
inhibitors, and SGLT2 inhibitors. The pathways affected by this health condition include
KEGG adipocytokine signaling pathways, biocarta prara pathway, and ST stat 3 pathways.
The progression starts with the functional deterioration of beta cells and leads to failure. And
inflammations some of the potential outcomes in that occurs are impairments to blood
vessels, legs, heart, mind, issues in kidney function, gums, teeth, skin sexual parts, and in
severe cases even cause death.
DIABETES
6
6
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Reference
Allin, K. H., Nielsen, T., & Pedersen, O. (2015). Mechanisms in endocrinology: gut
microbiota in patients with type 2 diabetes mellitus. European journal of
endocrinology, 172(4), R167-R177.
Chatterjee, S., Khunti, K. and Davies, M.J., 2017. Type 2 diabetes. The Lancet, 389(10085),
pp.2239-2251.
Dawed, A. Y., Donnelly, L., Tavendale, R., Carr, F., Leese, G., Palmer, C. N., & Zhou, K.
(2016). CYP2C8 and SLCO1B1 variants and therapeutic response to
thiazolidinediones in patients with type 2 diabetes. Diabetes Care, 39(11), 1902-1908.
Dooley, J., Tian, L., Schonefeldt, S., Delghingaro-Augusto, V., Garcia-Perez, J. E., Pasciuto,
E., & Franckaert, D. (2016). Genetic predisposition for beta cell fragility underlies
type 1 and type 2 diabetes. Nature Genetics, 48(5), 519.
Forslund, K., Hildebrand, F., Nielsen, T., Falony, G., Le Chatelier, E., Sunagawa, S., &
Arumugam, M. (2015). Disentangling type 2 diabetes and metformin treatment
signatures in the human gut microbiota. Nature, 528(7581), 262.
Marso, S. P., Daniels, G. H., Brown-Frandsen, K., Kristensen, P., Mann, J. F., Nauck, M. A.,
& Steinberg, W. M. (2016). Liraglutide and cardiovascular outcomes in type 2
diabetes. New England Journal of Medicine, 375(4), 311-322.
Scheen, A. J. (2015). Pharmacodynamics, efficacy, and safety of sodium–glucose co-
transporter type 2 (SGLT2) inhibitors for the treatment of type 2 diabetes mellitus.
Drugs, 75(1), 33-59.
7
Reference
Allin, K. H., Nielsen, T., & Pedersen, O. (2015). Mechanisms in endocrinology: gut
microbiota in patients with type 2 diabetes mellitus. European journal of
endocrinology, 172(4), R167-R177.
Chatterjee, S., Khunti, K. and Davies, M.J., 2017. Type 2 diabetes. The Lancet, 389(10085),
pp.2239-2251.
Dawed, A. Y., Donnelly, L., Tavendale, R., Carr, F., Leese, G., Palmer, C. N., & Zhou, K.
(2016). CYP2C8 and SLCO1B1 variants and therapeutic response to
thiazolidinediones in patients with type 2 diabetes. Diabetes Care, 39(11), 1902-1908.
Dooley, J., Tian, L., Schonefeldt, S., Delghingaro-Augusto, V., Garcia-Perez, J. E., Pasciuto,
E., & Franckaert, D. (2016). Genetic predisposition for beta cell fragility underlies
type 1 and type 2 diabetes. Nature Genetics, 48(5), 519.
Forslund, K., Hildebrand, F., Nielsen, T., Falony, G., Le Chatelier, E., Sunagawa, S., &
Arumugam, M. (2015). Disentangling type 2 diabetes and metformin treatment
signatures in the human gut microbiota. Nature, 528(7581), 262.
Marso, S. P., Daniels, G. H., Brown-Frandsen, K., Kristensen, P., Mann, J. F., Nauck, M. A.,
& Steinberg, W. M. (2016). Liraglutide and cardiovascular outcomes in type 2
diabetes. New England Journal of Medicine, 375(4), 311-322.
Scheen, A. J. (2015). Pharmacodynamics, efficacy, and safety of sodium–glucose co-
transporter type 2 (SGLT2) inhibitors for the treatment of type 2 diabetes mellitus.
Drugs, 75(1), 33-59.
DIABETES
8
Violi, F., Targher, G., Vestri, A., Carnevale, R., Averna, M., Farcomeni, A., Lenzi, A.,
Angelico, F., Cipollone, F. and Pastori, D., (2017). Effect of aspirin on renal disease
progression in patients with type 2 diabetes: A multicenter, double-blind, placebo-
controlled, randomized trial. The renaL disease progression by aspirin in diabetic
patients (LEDA) trial. Rationale and study design. American heart journal, 189,
pp.120-127.
Xin, C., Liu, J., Zhang, J., Zhu, D., Wang, H., Xiong, L., & Zhang, L. (2016). Irisin improves
fatty acid oxidation and glucose utilization in type 2 diabetes by regulating the AMPK
signaling pathway. International journal of obesity, 40(3), 443.
Yu, O., Azoulay, L., Yin, H., Filion, K. B., & Suissa, S. (2018). Sulfonylureas as initial
treatment for type 2 diabetes and the risk of severe hypoglycemia. The American
journal of medicine, 131(3), 317-e11.
Zaccardi, F., Webb, D. R., Yates, T., & Davies, M. J. (2016). Pathophysiology of type 1 and
type 2 diabetes mellitus: a 90-year perspective. The postgraduate medical
journal, 92(1084), 63-69.
8
Violi, F., Targher, G., Vestri, A., Carnevale, R., Averna, M., Farcomeni, A., Lenzi, A.,
Angelico, F., Cipollone, F. and Pastori, D., (2017). Effect of aspirin on renal disease
progression in patients with type 2 diabetes: A multicenter, double-blind, placebo-
controlled, randomized trial. The renaL disease progression by aspirin in diabetic
patients (LEDA) trial. Rationale and study design. American heart journal, 189,
pp.120-127.
Xin, C., Liu, J., Zhang, J., Zhu, D., Wang, H., Xiong, L., & Zhang, L. (2016). Irisin improves
fatty acid oxidation and glucose utilization in type 2 diabetes by regulating the AMPK
signaling pathway. International journal of obesity, 40(3), 443.
Yu, O., Azoulay, L., Yin, H., Filion, K. B., & Suissa, S. (2018). Sulfonylureas as initial
treatment for type 2 diabetes and the risk of severe hypoglycemia. The American
journal of medicine, 131(3), 317-e11.
Zaccardi, F., Webb, D. R., Yates, T., & Davies, M. J. (2016). Pathophysiology of type 1 and
type 2 diabetes mellitus: a 90-year perspective. The postgraduate medical
journal, 92(1084), 63-69.
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