Diabetes mellitus type 2 pathophysiology: Difference between revisions
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{{ | {{CMG}}; {{AE}} [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh13579@gmail.com]; {{CZ}} | ||
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==Pathophysiology== | ==Pathophysiology== | ||
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Revision as of 18:56, 6 July 2016
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Diabetes mellitus type 2 Microchapters |
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Differentiating Diabetes Mellitus Type 2 from other Diseases |
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Diagnosis |
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Treatment |
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Medical therapy |
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Diabetes mellitus Main page |
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Patient Information |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Priyamvada Singh, M.B.B.S. [2]; Cafer Zorkun, M.D., Ph.D. [3]
Overview
Pathophysiology
Insulin resistance means that body cells do not respond appropriately when insulin is present.
Other important contributing factors:
- increased hepatic glucose production (e.g., from glycogen degradation), especially at inappropriate times
- decreased insulin-mediated glucose transport in (primarily) muscle and adipose tissues (receptor and post-receptor defects)
- impaired beta-cell function—loss of early phase of insulin release in response to hyperglycemic stimuli
- Cancer survivors who received allogenic Hematopoeitic Cell Transplantation (HCT) are 3.65 times more likely to report type 2 diabetes than their siblings. Total body irradiation (TBI) is also associated with a higher risk of developing diabetes.
This is a more complex problem than type 1, but is sometimes easier to treat, especially in the initial years when insulin is often still being produced internally. Type 2 may go unnoticed for years in a patient before diagnosis, since the symptoms are typically milder (no ketoacidosis) and can be sporadic. However, severe complications can result from unnoticed type 2 diabetes, including renal failure, blindness, wounds that fail to heal, and coronary artery disease. The onset of the disease is most common in middle age and later life.
Diabetes mellitus type 2 is presently of unknown etiology (i.e., origin). Diabetes mellitus with a known etiology, such as secondary to other diseases, known gene defects, trauma or surgery, or the effects of drugs, is more appropriately called secondary diabetes mellitus. Examples include diabetes mellitus caused by hemochromatosis, pancreatic insufficiency, or certain types of medications (e.g. long-term steroid use).
About 90–95% of all North American cases of diabetes are type 2[1], and about 20% of the population over the age of 65 has diabetes mellitus type 2. The fraction of type 2 diabetics in other parts of the world varies substantially, almost certainly for environmental and lifestyle reasons, though these are not known in detail. Diabetes affects over 150 million people worldwide with this number expected to double by 2025[1]. There is also a strong inheritable genetic connection in type 2 diabetes: having relatives (especially first degree) with type 2 is a considerable risk factor for developing type 2 diabetes. In addition there is also a mutation to the Islet Amyloid Polypeptide gene that results in an earlier onset, more severe form of diabetes[2],[3]. About 55 percent of type 2 are obese[4] —chronic obesity leads to increased insulin resistance that can develop into diabetes, most likely because adipose tissue is a (recently identified) source of chemical signals (hormones and cytokines). Other research shows that type 2 diabetes causes obesity.[5]
Diabetes mellitus type 2 is often associated with obesity and hypertension and elevated cholesterol (combined hyperlipidemia), and with the condition Metabolic syndrome (also known as Syndrome X, Reavan's syndrome, or CHAOS). It is also associated with acromegaly, Cushing's syndrome and a number of otherendocrinological disorders. Additional factors found to increase risk of type 2 diabetes include aging[6], high-fat diets[7] and a less active lifestyle[8].
References
- ↑ 1.0 1.1 Zimmet, P., Alberti, K. G. M. M., Shaw, J. Global and societal implications of the diabetes epidemic. Nature 2001, 414, 782-787.
- ↑ Sakagashira, S., Sanke, T., Hanabusa, T., Shimomura, H., Ohagi, S., Kumagaye, K. Y.,Nakajima, K. & Nanjo, K. Missense mutation of amylin gene (S20G) in Japanese NIDDM patients. Diabetes 1996, 45, 1279-1281.
- ↑ Seino, S. S20G mutation of the amylin gene is associated with Type II diabetes in Japanese. Diabetologia 2001, 44, (7), 906-909.
- ↑ Eberhart, M. S. (November 19, 2004). "Prevalence of Overweight and Obesity Among Adults with Diagnosed Diabetes --- United States, 1988--1994 and 1999--2002". Morbidity and Mortality Weekly Report. Centers for Disease Control and Prevention. 53 (45): 1066–1068. Unknown parameter
|coauthors=ignored (help) - ↑ Camastra S, Bonora E, Del Prato S, Rett K, Weck M, Ferrannini E (1999). "Effect of obesity and insulin resistance on resting and glucose-induced thermogenesis in man. EGIR (European Group for the Study of Insulin Resistance)". Int J Obes Relat Metab Disord. 23 (12): 1307–13. PMID 10643689.
- ↑ Jack, L., Jr., Boseman, L. & Vinicor, F. Aging Americans and diabetes. A public health and clinical response. Geriatrics 2004, 59, 14-17.
- ↑ Lovejoy, J. C. The influence of dietary fat on insulin resistance. Curr Diab Rep 2002, 2,435-440.
- ↑ Hu, F. B. Sedentary lifestyle and risk of obesity and type 2 diabetes. Lipids 2003, 38,103-108.