Diabetes mellitus type 2 formerly non-insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes is a metabolic disorder that is characterized by high

gh blood glucose in the context of insulin resistance and relative insulin deficiency.[2] The classic symptoms are excess thirst, frequent urination, and constant hunger. Type 2 diabetes makes up about 90% of cases of diabetes with the other 10% due primarily to diabetes mellitus type 1 and gestational diabetes. Obesity is thought to be the primary cause of type 2 diabetes in people who are genetically predisposed to the disease. Type 2 diabetes is initially managed by increasing exercise and dietary modification. If blood glucose levels are not adequately lowered by these measures, medications such as metformin or insulin may be needed. In those on insulin there is typically the requirement to routinely check blood sugar levels. Rates of diabetes have increased markedly over the last 50 years in parallel with obesity. As of 2010 there are approximately 285 million people with the disease compared to around 30 million in 1985. Long-term complications from high blood sugar can include heart attacks, strokes, diabetic retinopathy where eyesight is affected, kidney failure which may require dialysis, and poor circulation of limbs leading to amputations. The acute complication ketoacidosis is uncommon unlike in type 1 diabetes,[3] nonketonic hyperglycemia however may occur.

Contents
[hide]

1 Signs and symptoms o 1.1 Complications 2 Cause o 2.1 Lifestyle o 2.2 Genetics o 2.3 Medical conditions 3 Pathophysiology 4 Diagnosis 5 Screening 6 Prevention 7 Management o 7.1 Lifestyle o 7.2 Medications o 7.3 Surgery 8 Epidemiology 9 History 10 References 11 External links

[edit] Signs and symptoms

Overview of the most significant symptoms of diabetes. The classic symptoms of diabetes are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss.[4]

[edit] Complications
Main article: Complications of diabetes mellitus Type 2 diabetes is typically a chronic disease, associated with a ten year shorter life expectancy.[5] This is partly due to a number of complications with which it is associated including: two to four times the risk of cardiovascular disease and stroke, a 20 fold increase in lower limb amputations, and increased rates of hospitalizations.[5] In the developed world, and increasingly elsewhere, type 2 diabetes is the largest cause of non-traumatic blindness and kidney failure, as compared to non-diabetics.[6] It has also been associated with an increased risk of cognitive dysfunction and dementia through disease processes such as Alzheimer's disease and vascular dementia.[7] Other complications include: acanthosis nigricans, sexual dysfunction, and frequent infections.[4]

[edit] Cause
The development of type 2 diabetes is caused by a combination of lifestyle and genetic factors.[6][8] While some are under personal control such as diet and obesity others such as age, gender, and genetics are not.[5] A lack of sleep has been linked to type 2 diabetes[9] as has nutritional status during fetal development.[10]

[edit] Lifestyle
Main article: Lifestyle causes of diabetes mellitus type 2 A number of lifestyle factors are known to be important to the development of type 2 diabetes including: obesity, lack of sufficient physical activity, poor diet, stress, and urbanization.[5]

Excess body fat is associated with 64% of cases of diabetes in men and 77% of cases in women.[11] A number of dietary factors such as consumption of sugar sweetened drinks in excess [12][13] and the type of fats in the diet appear to play a role.[8]

[edit] Genetics
Main article: Genetic causes of diabetes mellitus type 2 Most cases of diabetes involve many genes with each being a small contributor to an increased probability of becoming a Type 2 diabetic.[5] As of 2011, more than 36 genes have been found that contribute to the risk of type 2 diabetes.[14] All of these genes together still only account for 10% of the total genetic component of the disease.[14] There are a number of rare cases of diabetes that arise due to an abnormality in a single gene (known as monogenic forms of diabetes).[5] These include maturity onset diabetes of the young (MODY), Donohue syndrome, and Rabson-Mendenhall syndrome, among others.[5] Maturity onset diabetes of the young constitute 15 % of all cases of diabetes in young people.[15]

[edit] Medical conditions

There are a number of medications and other health problems that can predispose to diabetes.[16] Some of the medications include: glucocorticoids, thiazides, beta-adrenergic agonist, alpha interferon.[16] Those who have previously had gestational diabetes are at a higher risk of developing type 2 diabetes.[4] Other health problems that are associated include: acromegaly, Cushing's syndrome, hyperthyroidism, pheochromocytoma, and certain cancers such as glucagonomas.[16] Testosterone deficiency is also associated with type 2 diabetes.[17][18]

[edit] Pathophysiology
Type 2 diabetes is due to insulin resistance primarily within the muscles and fat tissue and, in progressive cases, eventually inadequate insulin production from the beta cells to compensate.[19] This occurs in combination with inappropriate glucose release from the liver, which is controlled by blood insulin levels, and thus results in the classic finding of high blood sugar.[5] Other potential important mechanisms include: increased break down of lipids with in the fat cell, resistance to and lack of incretin, high glucagon levels in the blood, increased absorption of fluids in the kidneys, and the central nervous system not appropriately regulating metabolism.[5]

[edit] Diagnosis
Diabetes diagnostic criteria[20][21] edit Condition 2 hour glucose Fasting glucose HbA1c mmol/l(mg/dl) mmol/l(mg/dl) % Normal <7.8 (<140) <6.1 (<110) <6.0 Impaired fasting glycaemia <7.8 (<140) 6.1(110) & <7.0(<126) 6.0-6.4

Impaired glucose tolerance Diabetes mellitus

7.8 (140) 11.1 (200)

<7.0 (<126) 7.0 (126)

6.0-6.4 6.5

The World Health Organization definition of diabetes is for a single raised glucose reading with symptoms, otherwise raised values on two occasions, of either:[22]

fasting plasma glucose 7.0 mmol/l (126 mg/dl) or

with a glucose tolerance test, two hours after the oral dose a plasma glucose 11.1 mmol/l (200 mg/dl)

A glycated hemoglobin (HbA1c) of greater than 6.5% is another method of diagnosing diabetes[5] as is a random blood sugar of greater than 11.1 mmol/l (200 mg/dL) in association with typical symptoms.[4] These cut off have been decided based on the fact that complications such as retinal problems begin to increase at greater values.[5] A fasting or random blood sugar is preferred over the glucose tolerance test for most diagnosis as they are more convenient for people.[5] It is estimated that 20% of people with diabetes in the United States do not realize that they have the disease.[5]

[edit] Screening
No major organization recommends universal screening for diabetes as there is no evidence that such a program would improve outcomes.[23] Screening is recommended by the United States Preventive Services Task Force in adults without symptoms whose blood pressure is greater than 135/80 mmHg.[24] For those whose blood pressure is less, the evidence is insufficient to recommend for or against screening.[24] The World Health Organization recommends only testing those groups at high risk.[23] High risk groups in the United States include: those over 45 years old, those with a first degree relative with diabetes, some ethnic groups including Hispanics, African-Americans, and Native-Americans, a history of gestational diabetes, polycystic ovary syndrome, excess weight, and conditions associated with metabolic syndrome.[4]

[edit] Prevention
Main article: Prevention of diabetes mellitis type 2 Onset of type 2 diabetes can be delayed or prevented through proper nutrition and regular exercise.[25][26] Intensive lifestyle measures may reduce the risk by over half.[6] The benefit of exercise occur regardless of the persons initial weight or subsequent weight loss.[27] Evidence for the benefit of dietary changes alone however is limited;[28] with some evidence for a diet high in green leafy vegetables[29] and some for limiting the intake of sugary drinks.[12] In those with impaired glucose tolerance, diet and exercise and/or metformin or acarbose may decrease the risk of developing diabetes.[6][30] Lifestyle interventions are more effective than metformin.[6]

[edit] Management
Further information: Diabetes management Management of type 2 diabetes focuses on lifestyle interventions, lowering other cardiovascular risk factors, and maintaining blood glucose levels in the normal range.[6] Self-monitoring of blood glucose for people with newly diagnosed type 2 diabetes was recommended by the National Health Services in 2008,[31] however the benefit of self monitoring in those not using multi-dose insulin is questionable.[6] Managing other cardiovascular risk factors including hypertension, high cholesterol, and microalbuminuria improves a person's life expectancy.[6] Intensive blood sugar lowering as opposed to standard blood sugar lowering does not appear to change mortality.[32] The goal of treatment is typically an HbA1C of less than 7% or a fasting glucose of less than 6.7 mmol/L (120 mg/dL) however these goals may be changed after professional clinical consultation, taking into account particular risks of hypoglycemia and life expectancy.[4]

[edit] Lifestyle
A proper diet and exercise are the foundations of diabetic care[4] with a greater amount of exercise yielding better results.[33] Aerobic exercise leads to a decrease in HbA1C and improved insulin sensitivity.[33] Resistance training is also useful and the combination of both types of exercise may be most effective.[33] A diabetic diet that promotes weight loss is important.[34] While the best diet type to achieve this is controversial[34] a low glycemic index diet has been found to improve blood sugar control.[35] Culturally appropriate education may help people with Type 2 diabetes control their blood sugar levels, for up to six months at least.[36] If lifestyle measures in those with mildly elevated blood sugars have not resulted in an improvement within six weeks medications should than be considered.[4]

[edit] Medications

Metformin 500mg tablets There are several classes of anti-diabetic medications available. Metformin is generally recommended as a first line treatment as there is good evidence that it decreases mortality.[6]

Injections of insulin may either be added to oral medication or used alone.[6] Other classes of medications used to treat type 2 diabetes are sulfonylureas, nonsulfonylurea secretagogues, alpha glucosidase inhibitors, and thiazolidinediones.[6] Metformin however should not be used in those with severe kidney or liver problems.[4] When insulin is used, a long-acting formulation is typically added initially at night, while oral medications are continued.[4][6] Doses are then increased to effect.[6] When nightly insulin is insufficient twice daily insulin may achieve better control.[4] The long acting insulins, glargine and detemir, do not appear much better than NPH but have a significantly greater cost making them as of 2010 not cost effective.[37] In those who are pregnant insulin is generally the treatment of choice.[4]

[edit] Surgery
Weight loss surgery in those who are obese appears to be an effective measure to treat diabetes.[38] Many are able to maintain normal blood sugar levels with little or no medications following surgery[39] and long term mortality is decreased.[40] There however is some short term mortality risk of less than 1% from the surgery.[41] The body mass index cutoffs for when surgery is appropriate are not yet clear.[40]

[edit] Epidemiology

Prevalence of diabetes worldwide in 2000 (per 1000 inhabitants). World average was 2.8%. no data 4552.5 7.5 52.560 7.515 6067.5 1522.5 67.575 22.530 7582.5 3037.5 82.5 37.545 Globally as of 2010 it is estimated that there are 285 million people with type 2 diabetes making up about 90% of diabetes cases.[5] This is equivalent to about 6% of the worlds adult population.[42] It is common both in the developed and the developing world.[5] Women seem to be at a greater risk as do certain ethnic groups[5] such as Pacific Islanders, Latinos, and Native Americans.[4] This may be due to certain ethnic group's sensitivity to a Western lifestyle.[43] Traditionally considered a disease of adults, type 2 diabetes is increasingly diagnosed in children in parallel to rising obesity rates.[5]

Rates of diabetes in 1985 were estimated at 30 million, increasing to 135 million in 1995 and 217 million in 2005.[44] This increase is believed to be primarily due to the global population aging, a decrease in exercise, and increasing rates of obesity.[44] It is recognized as a global epidemic by the World Health Organization.[45]

[edit] History
Main article: History of diabetes Diabetes is one of the first diseases described[46] with an Egyptian manuscript from c. 1500 BCE mentioning too great emptying of the urine.[47] The first described cases are believed to be of type 1 diabetes.[47] Indian physicians around the same time identified the disease and classified it as madhumeha or honey urine noting that the urine would attract ants.[47] The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Appollonius Of Memphis.[47] The disease was rare during the time of the Roman empire with Galen commenting that he had only seen two cases during his career.[47] Type 1 and type 2 diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400-500 AD with type 1 associated with youth and type 2 with being overweight.[47] The term "mellitus" or "from honey" was added by the Britain John Rolle in the late 1700s to separate the condition from diabetes insipidus which is also associated with frequent urination.[47] While many measure where tried effective treatment was not developed until the early part of the 20th century when the Canadians Frederick Banting and Charles Best developed insulin in 1921 and 1922.[47] This was followed by the development of the long acting insulin NPH in the 1940s.[47]

[edit] References
1. ^ "Diabetes Blue Circle Symbol". International Diabetes Federation. 17 March 2006. http://www.diabetesbluecircle.org. 2. ^ Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Cotran, Ramzi S. ; Robbins, Stanley L. (2005). Robbins and Cotran Pathologic Basis of Disease (7th ed.). Philadelphia, Pa.: Saunders. pp. 11941195. ISBN 0-7216-0187-1. 3. ^ Fasanmade, OA; Odeniyi, IA, Ogbera, AO (2008 Jun). "Diabetic ketoacidosis: diagnosis and management". African journal of medicine and medical sciences 37 (2): 99105. PMID 18939392. 4. ^ a b c d e f g h i j k l m Vijan, S (2010-03-02). "Type 2 diabetes". Annals of internal medicine 152 (5): ITC3115; quiz ITC316. doi:10.1059/0003-4819-152-5-201003020-01003. PMID 20194231. 5. ^ a b c d e f g h i j k l m n o p q Williams textbook of endocrinology. (12th ed.). Philadelphia: Elsevier/Saunders. pp. 13711435. ISBN 978-1437703245. 6. ^ a b c d e f g h i j k l m Ripsin CM, Kang H, Urban RJ (January 2009). "Management of blood glucose in type 2 diabetes mellitus". Am Fam Physician 79 (1): 2936. PMID 19145963. 7. ^ Pasquier, F (2010 Oct). "Diabetes and cognitive impairment: how to evaluate the cognitive status?". Diabetes & metabolism 36 Suppl 3: S1005. doi:10.1016/S12623636(10)70475-4. PMID 21211730.

8. ^ a b Risrus U, Willett WC, Hu FB (January 2009). "Dietary fats and prevention of type 2 diabetes". Progress in Lipid Research 48 (1): 4451. doi:10.1016/j.plipres.2008.10.002. PMC 2654180. PMID 19032965. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2654180. 9. ^ Touma, C; Pannain, S (2011 Aug). "Does lack of sleep cause diabetes?". Cleveland Clinic journal of medicine 78 (8): 54958. doi:10.3949/ccjm.78a.10165. PMID 21807927. 10. ^ Christian, P; Stewart, CP (2010 Mar). "Maternal micronutrient deficiency, fetal development, and the risk of chronic disease". The Journal of nutrition 140 (3): 43745. doi:10.3945/jn.109.116327. PMID 20071652. 11. ^ Peter G. Kopelman, Ian D. Caterson, Michael J. Stock, William H. Dietz (2005). Clinical obesity in adults and children: In Adults and Children. Blackwell Publishing. pp. 9. ISBN 140-511672-2. 12. ^ a b Malik, VS; Popkin, BM, Bray, GA, Desprs, JP, Hu, FB (2010-03-23). "Sugar Sweetened Beverages, Obesity, Type 2 Diabetes and Cardiovascular Disease risk". Circulation 121 (11): 135664. doi:10.1161/CIRCULATIONAHA.109.876185. PMC 2862465. PMID 20308626. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2862465. 13. ^ Malik, VS; Popkin, BM, Bray, GA, Desprs, JP, Willett, WC, Hu, FB (2010 Nov). "Sugar-Sweetened Beverages and Risk of Metabolic Syndrome and Type 2 Diabetes: A meta-analysis". Diabetes care 33 (11): 247783. doi:10.2337/dc10-1079. PMC 2963518. PMID 20693348. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2963518. 14. ^ a b Herder, C; Roden, M (2011 Jun). "Genetics of type 2 diabetes: pathophysiologic and clinical relevance". European journal of clinical investigation 41 (6): 67992. doi:10.1111/j.1365-2362.2010.02454.x. PMID 21198561. 15. ^ "Monogenic Forms of Diabetes: Neonatal Diabetes Mellitus and Maturity-onset Diabetes of the Young". National Diabetes Information Clearinghouse (NDIC) (National Institute of Diabetes and Digestive and Kidney Diseases, NIH). http://www.diabetes.niddk.nih.gov/dm/pubs/mody/. Retrieved 2008-08-04. 16. ^ a b c Bethel, edited by Mark N. Feinglos, M. Angelyn (2008). Type 2 diabetes mellitus : an evidence-based approach to practical management. Totowa, NJ: Humana Press. pp. 462. ISBN 9781588297945. http://books.google.ca/books?id=NctBmHUOV7AC&pg=PA462. 17. ^ Saad F, Gooren L (March 2009). "The role of testosterone in the metabolic syndrome: a review". The Journal of Steroid Biochemistry and Molecular Biology 114 (12): 403. doi:10.1016/j.jsbmb.2008.12.022. PMID 19444934. 18. ^ Farrell JB, Deshmukh A, Baghaie AA (2008). "Low testosterone and the association with type 2 diabetes". The Diabetes Educator 34 (5): 799806. doi:10.1177/0145721708323100. PMID 18832284. 19. ^ McCarthy, MI; Guttmacher, Alan E.; McCarthy, Mark I. (2010-12-09). "Genomics, type 2 diabetes, and obesity". The New England journal of medicine 363 (24): 233950. doi:10.1056/NEJMra0906948. PMID 21142536. 20. ^ "Definition and Diagnosis of Diabetes Mellitus and Intermediate Hyperglycemia" (pdf). World Health Organization. www.who.int. 2006.

http://www.who.int/diabetes/publications/Definition%20and%20diagnosis%20of%20dia betes_new.pdf. Retrieved 2011-02-20. 21. ^ Vijan, S (2010 Mar 2). "Type 2 diabetes.". Annals of internal medicine 152 (5): ITC3115; quiz ITC316. PMID 20194231. 22. ^ World Health Organization. "Definition, diagnosis and classification of diabetes mellitus and its complications: Report of a WHO Consultation. Part 1. Diagnosis and classification of diabetes mellitus". http://www.who.int/diabetes/publications/en/. Retrieved 29 May 2007. 23. ^ a b Valdez R (2009). "Detecting Undiagnosed Type 2 Diabetes: Family History as a Risk Factor and Screening Tool". J Diabetes Sci Technol 3 (4): 7226. PMC 2769984. PMID 20144319. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2769984. 24. ^ a b "Screening: Type 2 Diabetes Mellitus in Adults". U.S. Preventive Services Task Force. 2008. http://www.uspreventiveservicestaskforce.org/uspstf/uspsdiab.htm. 25. ^ Raina Elley C, Kenealy T (December 2008). "Lifestyle interventions reduced the longterm risk of diabetes in adults with impaired glucose tolerance". Evid Based Med 13 (6): 173. doi:10.1136/ebm.13.6.173. PMID 19043031. 26. ^ Orozco LJ, Buchleitner AM, Gimenez-Perez G, Roqu I Figuls M, Richter B, Mauricio D (2008). Mauricio, Didac. ed. "Exercise or exercise and diet for preventing type 2 diabetes mellitus". Cochrane Database Syst Rev (3): CD003054. doi:10.1002/14651858.CD003054.pub3. PMID 18646086. 27. ^ O'Gorman, DJ; Krook, A (2011 Sep). "Exercise and the treatment of diabetes and obesity". The Medical clinics of North America 95 (5): 95369. doi:10.1016/j.mcna.2011.06.007. PMID 21855702. 28. ^ Nield L, Summerbell CD, Hooper L, Whittaker V, Moore H (2008). Nield, Lucie. ed. "Dietary advice for the prevention of type 2 diabetes mellitus in adults". Cochrane Database Syst Rev (3): CD005102. doi:10.1002/14651858.CD005102.pub2. PMID 18646120. 29. ^ Carter, P; Gray, LJ, Troughton, J, Khunti, K, Davies, MJ (2010-08-18). "Fruit and vegetable intake and incidence of type 2 diabetes mellitus: systematic review and metaanalysis". BMJ (Clinical research ed.) 341: c4229. doi:10.1136/bmj.c4229. PMC 2924474. PMID 20724400. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2924474. 30. ^ Santaguida PL, Balion C, Hunt D, et al. (August 2005). "Diagnosis, prognosis, and treatment of impaired glucose tolerance and impaired fasting glucose" (PDF). Evid Rep Technol Assess (Summ) (128): 111. PMID 16194123. http://www.ahrq.gov/downloads/pub/evidence/pdf/impglucose/impglucose.pdf. 31. ^ "Clinical Guideline:The management of type 2 diabetes (update)". http://www.nice.org.uk/guidance/index.jsp?action=byID&o=11983. 32. ^ Boussageon, R; Bejan-Angoulvant, T, Saadatian-Elahi, M, Lafont, S, Bergeonneau, C, Kassa, B, Erpeldinger, S, Wright, JM, Gueyffier, F, Cornu, C (2011-07-26). "Effect of intensive glucose lowering treatment on all cause mortality, cardiovascular death, and microvascular events in type 2 diabetes: meta-analysis of randomised controlled trials". BMJ (Clinical research ed.) 343: d4169. doi:10.1136/bmj.d4169. PMC 3144314. PMID 21791495. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3144314.

33. ^ a b c Zanuso S, Jimenez A, Pugliese G, Corigliano G, Balducci S (March 2010). "Exercise for the management of type 2 diabetes: a review of the evidence". Acta Diabetol 47 (1): 1522. doi:10.1007/s00592-009-0126-3. PMID 19495557. 34. ^ a b Davis N, Forbes B, Wylie-Rosett J (June 2009). "Nutritional strategies in type 2 diabetes mellitus". Mt. Sinai J. Med. 76 (3): 25768. doi:10.1002/msj.20118. PMID 19421969. 35. ^ Thomas D, Elliott EJ (2009). Thomas, Diana. ed. "Low glycaemic index, or low glycaemic load, diets for diabetes mellitus". Cochrane Database Syst Rev (1): CD006296. doi:10.1002/14651858.CD006296.pub2. PMID 19160276. 36. ^ Hawthorne, K.; Robles, Y.; Cannings-John, R.; Edwards, A. G. K.; Robles, Yolanda (2008). Robles, Yolanda. ed. "Culturally appropriate health education for Type 2 diabetes mellitus in ethnic minority groups". Cochrane Database Syst Rev (3): CD006424. doi:10.1002/14651858.CD006424.pub2. PMID 18646153. CD006424. 37. ^ Waugh, N; Cummins, E, Royle, P, Clar, C, Marien, M, Richter, B, Philip, S (2010 Jul). "Newer agents for blood glucose control in type 2 diabetes: systematic review and economic evaluation". Health technology assessment (Winchester, England) 14 (36): 1 248. doi:10.3310/hta14360. PMID 20646668. 38. ^ Picot, J; Jones, J, Colquitt, JL, Gospodarevskaya, E, Loveman, E, Baxter, L, Clegg, AJ (2009 Sep). "The clinical effectiveness and cost-effectiveness of bariatric (weight loss) surgery for obesity: a systematic review and economic evaluation". Health technology assessment (Winchester, England) 13 (41): 1190, 215357, iiiiv. doi:10.3310/hta13410. PMID 19726018. 39. ^ Frachetti, KJ; Goldfine, AB (2009 Apr). "Bariatric surgery for diabetes management". Current opinion in endocrinology, diabetes, and obesity 16 (2): 11924. doi:10.1097/MED.0b013e32832912e7. PMID 19276974. 40. ^ a b Schulman, AP; del Genio, F, Sinha, N, Rubino, F (2009 Sep-Oct). ""Metabolic" surgery for treatment of type 2 diabetes mellitus". Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists 15 (6): 62431. doi:10.4158/EP09170.RAR. PMID 19625245. 41. ^ Colucci, RA (2011 Jan). "Bariatric surgery in patients with type 2 diabetes: a viable option". Postgraduate medicine 123 (1): 2433. doi:10.3810/pgm.2011.01.2242. PMID 21293081. 42. ^ Meetoo, D; McGovern, P, Safadi, R (2007 Sep 13-27). "An epidemiological overview of diabetes across the world". British journal of nursing (Mark Allen Publishing) 16 (16): 10027. PMID 18026039. 43. ^ Carulli, L; Rondinella, S, Lombardini, S, Canedi, I, Loria, P, Carulli, N (2005 Nov). "Review article: diabetes, genetics and ethnicity". Alimentary pharmacology & therapeutics 22 Suppl 2: 169. doi:10.1111/j.1365-2036.2005.02588.x. PMID 16225465. 44. ^ a b Smyth, S; Heron, A (2006 Jan). "Diabetes and obesity: the twin epidemics". Nature medicine 12 (1): 7580. doi:10.1038/nm0106-75. PMID 16397575. 45. ^ "Diabetes Fact sheet N312". World Health Organization. Aug 2011. http://www.who.int/mediacentre/factsheets/fs312/en/. Retrieved 9 January 2012. 46. ^ Ripoll, Brian C. Leutholtz, Ignacio (2011-04-25). Exercise and disease management (2nd ed.). Boca Raton: CRC Press. pp. 25. ISBN 9781439827598. http://books.google.ca/books?id=eAn9-bm_pi8C&pg=PA25.

47. ^ a b c d e f g h i editor, Leonid Poretsky, (2009). Principles of diabetes mellitus (2nd ed.). New York: Springer. pp. 3. ISBN 9780387098401. http://books.google.ca/books?id=i0qojvF1SpUC&pg=PA3.

[edit] External links

Find more about Diabetes mellitus on Wikipedia's sister projects: Definitions and translations from Wiktionary Images and media from Commons Learning resources from Wikiversity News stories from Wikinews Quotations from Wikiquote Source texts from Wikisource Textbooks from Wikibooks

Diabetes mellitus type 2 at the Open Directory Project Type 2 Diabetes - General Information National Diabetes Information Clearinghouse Centers for Disease Control (Endocrine pathology) Clinical practice guidelines 2012 [show]

v t e

Endocrine pathology: endocrine diseases (E00E35, 240259)

Diabetes mellitus types: (type 1, type 2, MODY 1 2 3 4 5 6) complications (coma, angiopathy, Hypofunction ketoacidosis, nephropathy, neuropathy, retinopathy, cardiomyopathy) insulin receptor (RabsonMendenhall syndrome) Insulin resistance Hyperfunction Hypoglycemia beta cell (Hyperinsulinism) G cell (ZollingerEllison syndrome)

gonadotropin (Kallmann syndrome, Adiposogenital dystrophy) CRH (Tertiary Hypothalamus adrenal insufficiency) vasopressin (Neurogenic diabetes insipidus) general (Hypothalamic hamartoma) Pituitary anterior (Acromegaly, Hyperprolactinaemia, Pituitary ACTH Hyperpituitarism hypersecretion) posterior (SIADH) general (Nelson's syndrome)

anterior (Kallmann syndrome, Growth hormone deficiency, ACTH deficiency/Secondary adrenal insufficiency) Hypopituitarism posterior (Neurogenic diabetes insipidus) general (Empty sella syndrome, Pituitary apoplexy, Sheehan's syndrome, Lymphocytic hypophysitis) Hypothyroidism Iodine deficiency Cretinism (Congenital hypothyroidism) Myxedema Euthyroid sick syndrome

Hyperthyroxinemia (Thyroid hormone resistance, Familial Hyperthyroidism dysalbuminemic hyperthyroxinemia) Hashitoxicosis Thyrotoxicosis factitia Graves' disease Thyroid Thyroiditis Acute infectious Subacute (De Quervain's, Subacute lymphocytic) Autoimmune/chronic (Hashimoto's, Postpartum, Riedel's) Endemic goitre Toxic nodular goitre Toxic multinodular goiter Thyroid nodule

Goitre

Parathyroid

Hypoparathyroidism Pseudohypoparathyroidism Hyperparathyroidism Primary Secondary Tertiary Osteitis fibrosa cystica aldosterone: Hyperaldosteronism/Primary aldosteronism (Conn syndrome, Bartter syndrome, Glucocorticoid remediable Hyperfunction aldosteronism) AME Liddle's syndrome 17 CAH cortisol: Cushing's syndrome (Pseudo-Cushing's syndrome) sex hormones: 21 CAH 11 CAH Hypofunction/ aldosterone: Hypoaldosteronism (21 CAH, 11 CAH) Adrenal insufficiency cortisol: CAH (Lipoid, 3, 11, 17, 21) (Addison's, sex hormones: 17 CAH WF) ovarian: Polycystic ovary syndrome Premature ovarian failure testicular: enzymatic (5-alpha-reductase deficiency, 17-beta-hydroxysteroid dehydrogenase deficiency) Androgen receptor (Androgen insensitivity syndrome) general: Hypogonadism (Delayed puberty) Hypergonadism (Precocious puberty)

Adrenal

Gonads

M: END

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Diabetes (E10E14, 250)

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Alcohol and health

Sobriety Teetotalism Alcoholics Anonymous Temperance movement Alcohol detoxification Alcohol rehabilitation

Alcohol limitation Recommended maximum intake of alcoholic beverages Alcohol anti- Cannabidiol (CBD) (neuroprotection) Cannabis sativa (speculative) Ibogaine addictive Salvia divinorum entheogens Alcohol and Christianity and alcohol (alcohol in the Bible) Islam and alcohol Prohibition religion

digestive system nervous system

Alcoholic liver cirrhosis Fatty liver Alcoholic hepatitis Alcoholic liver disease Gastritis Pancreatitis Delirium tremens Alcohol dementia Alcoholic hallucinosis Blackout (alcohol-related amnesia) Wernicke-Korsakoff syndrome

cardiovascular Alcohol and cardiovascular disease Alcoholic cardiomyopathy Alcoholic system

lung disease

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Performing your original search, status diabetes mellitus, in PubMed will retrieve 14591 records.

CMAJ. 2011 Sep 6;183(12):E803-8. Epub 2011 Jul 25.

Recent epidemiologic trends of diabetes mellitus among status Aboriginal adults.

Oster RT, Johnson JA, Hemmelgarn BR, King M, Balko SU, Svenson LW, Crowshoe L, Toth EL.

Source
Department of Medicine, University of Alberta, Edmonton, Alta. roster@ualberta.ca

Abstract
BACKGROUND: Little is known about longitudinal trends in diabetes mellitus among Aboriginal people in Canada. We compared the incidence and prevalence of diabetes, and its impact on mortality, among status Aboriginal adults and adults in the general population between 1995 and 2007. METHODS: We examined de-identified data from Alberta Health and Wellness administrative databases for status Aboriginal people (First Nations and Inuit people with treaty status) and members of the

general public aged 20 years and older who received a diagnosis of diabetes mellitus from Apr. 1, 1995, to Mar. 31, 2007. We calculated the incidence and prevalence of diabetes and mortality rate ratios by sex and ethnicity in 2007. We examined the average relative changes per year for longitudinal trends. RESULTS: The average relative change per year in the prevalence of diabetes showed a smaller increase over time in the Aboriginal population than in the general population (2.39 v. 4.09, p < 0.001). A similar finding was observed for the incidence of diabetes. In the Aboriginal population, we found that the increase in the average relative change per year was greater among men than among women (3.13 v. 1.88 for prevalence, p < 0.001; 2.60 v. 0.02 for incidence, p = 0.001). Mortality among people with diabetes decreased over time to a similar extent in both populations. Among people without diabetes, mortality decreased in the general population but was unchanged in the Aboriginal population (-1.92 v. 0.11, p = 0.04). Overall, mortality was higher in the Aboriginal population than in the general population regardless of diabetes status. INTERPRETATION: The increases in the incidence and prevalence of diabetes over the study period appeared to be slower in the status Aboriginal population than in the general population in Alberta, although the overall rates were higher in the Aboriginal population. Mortality decreased among people with diabetes in both populations but was higher overall in the Aboriginal population regardless of diabetes status.
PMID: 21788417 [PubMed - indexed for MEDLINE] PMCID: PMC3168663 Free PMC Article

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Publication Types, MeSH Terms, Grant Support

Publication Types

Research Support, Non-U.S. Gov't

MeSH Terms

Adult Aged Alberta/epidemiology Diabetes Mellitus/epidemiology* Diabetes Mellitus/ethnology* Female Humans Incidence Indians, North American/statistics & numerical data* Inuits/statistics & numerical data* Male Middle Aged Prevalence Regression Analysis

Grant Support

OTG-88588/Canadian Institutes of Health Research/Canada

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