Diabetes mellitus type 2 overview: Difference between revisions
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==Overview== | ==Overview== | ||
Diabetes mellitus type 2 (formerly called non [[insulin]]-dependent diabetes (NIDDM), obesity related diabetes, or adult-onset diabetes) is a [[metabolism|metabolic]] disorder that is primarily characterized by [[insulin resistance]], relative insulin deficiency, and [[hyperglycemia]]. The defective responsiveness of body tissues to insulin almost certainly involves the [[insulin receptor]] in cell membranes. In the early stage the predominant abnormality is reduced insulin sensitivity, characterized by elevated levels of insulin in the blood. At this stage hyperglycemia can be managed by engaging in exercise, modifying one's diet and [[Anti-diabetic drug|medication]]s that improve insulin sensitivity or reduce glucose production by the [[liver]]. As the disease progresses the impairment of insulin secretion worsens, and therapeutic replacement of insulin often becomes necessary. It is rapidly increasing in the developed world, and there is some evidence that this pattern will be followed in much of the rest of the world in coming years. The [[Centers for Disease Control and Prevention|CDC]] has characterized the increase as an [[epidemic]].<ref>{{Citation | Diabetes mellitus type 2 (formerly called non [[insulin]]-dependent diabetes (NIDDM), obesity related diabetes, or adult-onset diabetes) is a [[metabolism|metabolic]] disorder that is primarily characterized by [[insulin resistance]], relative insulin deficiency, and [[hyperglycemia]]. The defective responsiveness of body tissues to insulin almost certainly involves the [[insulin receptor]] in cell membranes. In the early stage the predominant abnormality is reduced insulin sensitivity, characterized by elevated levels of insulin in the blood. At this stage hyperglycemia can be managed by engaging in exercise, modifying one's diet and [[Anti-diabetic drug|medication]]s that improve insulin sensitivity or reduce glucose production by the [[liver]]. As the disease progresses the impairment of [[insulin]] secretion worsens, and therapeutic replacement of [[insulin]] often becomes necessary. It is rapidly increasing in the developed world, and there is some evidence that this pattern will be followed in much of the rest of the world in coming years. The [[Centers for Disease Control and Prevention|CDC]] has characterized the increase as an [[epidemic]].<ref>{{Citation | ||
| last =Gerberding | | last =Gerberding | ||
| first =Julie Louise | | first =Julie Louise | ||
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==Historical Perspective== | ==Historical Perspective== | ||
Diabetes mellitus is a well-recognized disease from ancient times. In 1812 [[diabetes mellitus]] became a recognized clinical entity in The New England Journal of Medicine and Surgery. In 1889, the [[pancreas]] was identified as playing a major role in the pathogenesis of the disease. The discovery of [[insulin]] in 1921 was a major turning point in the history of diabetes when Frederick Banting and Charles Best were able to reverse the diabetic state in dogs by injecting pancreatic isolate from healthy dogs. | Diabetes mellitus is a well-recognized disease from ancient times. In 1812 [[diabetes mellitus]] became a recognized clinical entity in The New England Journal of Medicine and Surgery. In 1889, the [[pancreas]] was identified as playing a major role in the [[pathogenesis]] of the disease. The discovery of [[insulin]] in 1921 was a major turning point in the history of diabetes when Frederick Banting and Charles Best were able to reverse the diabetic state in dogs by injecting pancreatic isolate from healthy dogs. | ||
==Classification== | ==Classification== | ||
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==Pathophysiology== | ==Pathophysiology== | ||
The underlying pathology is the development of [[insulin resistance]]. Contrary to type 1 diabetes, patients with type 2 diabetes sufficiently produce [[insulin]]; however, cellular response to the circulating insulin is diminished. The mechanism by which the [[insulin resistance]] develops is postulated to be influenced by both genetic and environmental factors. Environmental influences on the pathogenesis of type 2 DM include high glycemic diets, central obesity, older age, male gender, low-fiber diet, and high saturated fat diet. | |||
==Causes== | ==Causes== | ||
The underlying cause of type 2 diabetes is insulin resistance. The exact cacuse of insulin resistance is not known, however several theories exist. Central obesity, aging, and high glycemic diets are most commonly implicated in the development of type 2 diabetes. | The underlying cause of type 2 diabetes is [[insulin resistance]]. The exact cacuse of insulin resistance is not known, however several theories exist. Central obesity, aging, and high glycemic diets are most commonly implicated in the development of type 2 diabetes. | ||
==Differentiating Diabetes mellitus type 2 from other Diseases== | ==Differentiating Diabetes mellitus type 2 from other Diseases== | ||
Type 2 diabetes mellitus must be differentiated from other disorders that may present with polyuria, polydipsia, weight loss or weight gain. Such disorders may include other forms of diabetes mellitus (e.g. type 1 DM, MODY) or other endocrine disorders (e.g. hypothyroidism, cushings syndrome, wolfram syndrome, alstrom syndrome) or drug | Type 2 diabetes mellitus must be differentiated from other disorders that may present with [[polyuria]], [[polydipsia]], [[weight loss]] or [[weight gain]]. Such disorders may include other forms of diabetes mellitus (e.g. [[Diabetes mellitus type 1|type 1 DM]], [[MODY]]) or other endocrine disorders (e.g. [[hypothyroidism]], [[Cushing's syndrome|cushings syndrome]], [[wolfram syndrome]], [[alstrom syndrome]]) or drug that can cause hyperglycemia (e.g. [[glucocorticoids]]) | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
The prevalence of type 2 [[diabetes mellitus]] (DM) is well studied in the United States and other developed countries. However, worldwide there is a large variation in the results of the population studies in developing countries and particularly in rural areas with poor access to healthcare. For this reason, diabetes is estimated to be undiagnosed in approximately 50% of adults worldwide. In the United States, African Americans, Mexican Americans, American Indians and non-Hispanic blacks are at a higher risk of developing type 2 diabetes compared to non-Hispanic whites. It is more prevalent among those older than 65 years, although there is a growing tend of childhood-onset of the disease. In 2011, 335 million people were estimated to have type 2 diabetes and that number is on a trajectory to reach over 500 million people by 2050. These figures correlate with a prevalence of approximately 5000 and 7500 per 100,000 in 2011 and 2050, respectively. Type 2 diabetes is more prevalent among men than women and in countries with low to mid income levels compared to high income level countries. It is classified as a global epidemic that is growing in parallel to massive urbanization.<ref name="pmid27733282">{{cite journal| author=GBD 2015 Disease and Injury Incidence and Prevalence Collaborators| title=Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015. | journal=Lancet | year= 2016 | volume= 388 | issue= 10053 | pages= 1545-1602 | pmid=27733282 | doi=10.1016/S0140-6736(16)31678-6 | pmc=5055577 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27733282 }} </ref> | The prevalence of type 2 [[diabetes mellitus]] (DM) is well studied in the United States and other developed countries. However, worldwide there is a large variation in the results of the population studies in developing countries and particularly in rural areas with poor access to healthcare. For this reason, diabetes is estimated to be undiagnosed in approximately 50% of adults worldwide. In the United States, African Americans, Mexican Americans, American Indians and non-Hispanic blacks are at a higher risk of developing type 2 diabetes compared to non-Hispanic whites. It is more prevalent among those older than 65 years, although there is a growing tend of childhood-onset of the disease. In 2011, 335 million people were estimated to have type 2 diabetes and that number is on a trajectory to reach over 500 million people by 2050. These figures correlate with a prevalence of approximately 5000 and 7500 per 100,000 in 2011 and 2050, respectively. Type 2 diabetes is more prevalent among men than women and in countries with low to mid income levels compared to high income level countries. It is classified as a global epidemic that is growing in parallel to massive urbanization.<ref name="pmid27733282">{{cite journal| author=GBD 2015 Disease and Injury Incidence and Prevalence Collaborators| title=Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015. | journal=Lancet | year= 2016 | volume= 388 | issue= 10053 | pages= 1545-1602 | pmid=27733282 | doi=10.1016/S0140-6736(16)31678-6 | pmc=5055577 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27733282 }} </ref> | ||
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==Risk Factors== | ==Risk Factors== | ||
Common risk factors associated with development of type 2 diabetes include: positive family history, certain ethnicity, obesity, smoking, physical inactivity, poor dietary habits, certain drugs (.eg. [[glucocorticoids]]) and certain medical conditions that may result in weight gain and inactivity.<ref name="pmid23052052">{{cite journal |vauthors=Scott RA, Langenberg C, Sharp SJ, Franks PW, Rolandsson O, Drogan D, van der Schouw YT, Ekelund U, Kerrison ND, Ardanaz E, Arriola L, Balkau B, Barricarte A, Barroso I, Bendinelli B, Beulens JW, Boeing H, de Lauzon-Guillain B, Deloukas P, Fagherazzi G, Gonzalez C, Griffin SJ, Groop LC, Halkjaer J, Huerta JM, Kaaks R, Khaw KT, Krogh V, Nilsson PM, Norat T, Overvad K, Panico S, Rodriguez-Suarez L, Romaguera D, Romieu I, Sacerdote C, Sánchez MJ, Spijkerman AM, Teucher B, Tjonneland A, Tumino R, van der A DL, Wark PA, McCarthy MI, Riboli E, Wareham NJ |title=The link between family history and risk of type 2 diabetes is not explained by anthropometric, lifestyle or genetic risk factors: the EPIC-InterAct study |journal=Diabetologia |volume=56 |issue=1 |pages=60–9 |year=2013 |pmid=23052052 |pmc=4038917 |doi=10.1007/s00125-012-2715-x |url=}}</ref><ref name="pmid11118026">{{cite journal |vauthors=Meigs JB, Cupples LA, Wilson PW |title=Parental transmission of type 2 diabetes: the Framingham Offspring Study |journal=Diabetes |volume=49 |issue=12 |pages=2201–7 |year=2000 |pmid=11118026 |doi= |url=}}</ref><ref name="pmid12503980">{{cite journal |vauthors=Mokdad AH, Ford ES, Bowman BA, Dietz WH, Vinicor F, Bales VS, Marks JS |title=Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001 |journal=JAMA |volume=289 |issue=1 |pages=76–9 |year=2003 |pmid=12503980 |doi= |url=}}</ref><ref name="pmid21128002">{{cite journal |vauthors=Nguyen NT, Nguyen XM, Lane J, Wang P |title=Relationship between obesity and diabetes in a US adult population: findings from the National Health and Nutrition Examination Survey, 1999-2006 |journal=Obes Surg |volume=21 |issue=3 |pages=351–5 |year=2011 |pmid=21128002 |pmc=3040808 |doi=10.1007/s11695-010-0335-4 |url=}}</ref><ref name="pmid1737857">{{cite journal |vauthors=Friedman JE, Dohm GL, Leggett-Frazier N, Elton CW, Tapscott EB, Pories WP, Caro JF |title=Restoration of insulin responsiveness in skeletal muscle of morbidly obese patients after weight loss. Effect on muscle glucose transport and glucose transporter GLUT4 |journal=J. Clin. Invest. |volume=89 |issue=2 |pages=701–5 |year=1992 |pmid=1737857 |pmc=442905 |doi=10.1172/JCI115638 |url=}}</ref><ref name="pmid7988316">{{cite journal |vauthors=Chan JM, Rimm EB, Colditz GA, Stampfer MJ, Willett WC |title=Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men |journal=Diabetes Care |volume=17 |issue=9 |pages=961–9 |year=1994 |pmid=7988316 |doi= |url=}}</ref><ref name="pmid11063954">{{cite journal |vauthors=Manson JE, Ajani UA, Liu S, Nathan DM, Hennekens CH |title=A prospective study of cigarette smoking and the incidence of diabetes mellitus among US male physicians |journal=Am. J. Med. |volume=109 |issue=7 |pages=538–42 |year=2000 |pmid=11063954 |doi= |url=}}</ref><ref name="pmid2589303">{{cite journal |vauthors=Feskens EJ, Kromhout D |title=Cardiovascular risk factors and the 25-year incidence of diabetes mellitus in middle-aged men. The Zutphen Study |journal=Am. J. Epidemiol. |volume=130 |issue=6 |pages=1101–8 |year=1989 |pmid=2589303 |doi= |url=}}</ref><ref name="pmid7888928">{{cite journal |vauthors=Rimm EB, Chan J, Stampfer MJ, Colditz GA, Willett WC |title=Prospective study of cigarette smoking, alcohol use, and the risk of diabetes in men |journal=BMJ |volume=310 |issue=6979 |pages=555–9 |year=1995 |pmid=7888928 |pmc=2548937 |doi= |url=}}</ref><ref name="pmid16186287">{{cite journal |vauthors=Foy CG, Bell RA, Farmer DF, Goff DC, Wagenknecht LE |title=Smoking and incidence of diabetes among U.S. adults: findings from the Insulin Resistance Atherosclerosis Study |journal=Diabetes Care |volume=28 |issue=10 |pages=2501–7 |year=2005 |pmid=16186287 |doi= |url=}}</ref> | Common risk factors associated with development of type 2 diabetes include: positive family history, certain ethnicity, [[obesity]], [[smoking]], [[physical inactivity]], poor dietary habits, certain drugs (.eg. [[glucocorticoids]]) and certain medical conditions that may result in weight gain and inactivity.<ref name="pmid23052052">{{cite journal |vauthors=Scott RA, Langenberg C, Sharp SJ, Franks PW, Rolandsson O, Drogan D, van der Schouw YT, Ekelund U, Kerrison ND, Ardanaz E, Arriola L, Balkau B, Barricarte A, Barroso I, Bendinelli B, Beulens JW, Boeing H, de Lauzon-Guillain B, Deloukas P, Fagherazzi G, Gonzalez C, Griffin SJ, Groop LC, Halkjaer J, Huerta JM, Kaaks R, Khaw KT, Krogh V, Nilsson PM, Norat T, Overvad K, Panico S, Rodriguez-Suarez L, Romaguera D, Romieu I, Sacerdote C, Sánchez MJ, Spijkerman AM, Teucher B, Tjonneland A, Tumino R, van der A DL, Wark PA, McCarthy MI, Riboli E, Wareham NJ |title=The link between family history and risk of type 2 diabetes is not explained by anthropometric, lifestyle or genetic risk factors: the EPIC-InterAct study |journal=Diabetologia |volume=56 |issue=1 |pages=60–9 |year=2013 |pmid=23052052 |pmc=4038917 |doi=10.1007/s00125-012-2715-x |url=}}</ref><ref name="pmid11118026">{{cite journal |vauthors=Meigs JB, Cupples LA, Wilson PW |title=Parental transmission of type 2 diabetes: the Framingham Offspring Study |journal=Diabetes |volume=49 |issue=12 |pages=2201–7 |year=2000 |pmid=11118026 |doi= |url=}}</ref><ref name="pmid12503980">{{cite journal |vauthors=Mokdad AH, Ford ES, Bowman BA, Dietz WH, Vinicor F, Bales VS, Marks JS |title=Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001 |journal=JAMA |volume=289 |issue=1 |pages=76–9 |year=2003 |pmid=12503980 |doi= |url=}}</ref><ref name="pmid21128002">{{cite journal |vauthors=Nguyen NT, Nguyen XM, Lane J, Wang P |title=Relationship between obesity and diabetes in a US adult population: findings from the National Health and Nutrition Examination Survey, 1999-2006 |journal=Obes Surg |volume=21 |issue=3 |pages=351–5 |year=2011 |pmid=21128002 |pmc=3040808 |doi=10.1007/s11695-010-0335-4 |url=}}</ref><ref name="pmid1737857">{{cite journal |vauthors=Friedman JE, Dohm GL, Leggett-Frazier N, Elton CW, Tapscott EB, Pories WP, Caro JF |title=Restoration of insulin responsiveness in skeletal muscle of morbidly obese patients after weight loss. Effect on muscle glucose transport and glucose transporter GLUT4 |journal=J. Clin. Invest. |volume=89 |issue=2 |pages=701–5 |year=1992 |pmid=1737857 |pmc=442905 |doi=10.1172/JCI115638 |url=}}</ref><ref name="pmid7988316">{{cite journal |vauthors=Chan JM, Rimm EB, Colditz GA, Stampfer MJ, Willett WC |title=Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men |journal=Diabetes Care |volume=17 |issue=9 |pages=961–9 |year=1994 |pmid=7988316 |doi= |url=}}</ref><ref name="pmid11063954">{{cite journal |vauthors=Manson JE, Ajani UA, Liu S, Nathan DM, Hennekens CH |title=A prospective study of cigarette smoking and the incidence of diabetes mellitus among US male physicians |journal=Am. J. Med. |volume=109 |issue=7 |pages=538–42 |year=2000 |pmid=11063954 |doi= |url=}}</ref><ref name="pmid2589303">{{cite journal |vauthors=Feskens EJ, Kromhout D |title=Cardiovascular risk factors and the 25-year incidence of diabetes mellitus in middle-aged men. The Zutphen Study |journal=Am. J. Epidemiol. |volume=130 |issue=6 |pages=1101–8 |year=1989 |pmid=2589303 |doi= |url=}}</ref><ref name="pmid7888928">{{cite journal |vauthors=Rimm EB, Chan J, Stampfer MJ, Colditz GA, Willett WC |title=Prospective study of cigarette smoking, alcohol use, and the risk of diabetes in men |journal=BMJ |volume=310 |issue=6979 |pages=555–9 |year=1995 |pmid=7888928 |pmc=2548937 |doi= |url=}}</ref><ref name="pmid16186287">{{cite journal |vauthors=Foy CG, Bell RA, Farmer DF, Goff DC, Wagenknecht LE |title=Smoking and incidence of diabetes among U.S. adults: findings from the Insulin Resistance Atherosclerosis Study |journal=Diabetes Care |volume=28 |issue=10 |pages=2501–7 |year=2005 |pmid=16186287 |doi= |url=}}</ref> | ||
==Screening== | ==Screening== | ||
Diabetes screening is recommended for many people at various stages of life, and for those with any of several risk factors. Screening tests are the same tests used for diagnosis. Early diagnosis and treatment can control the complications and result in better clinical outcomes. | Diabetes screening is recommended for many people at various stages of life, and for those with any of several risk factors. Screening tests are the same tests used for diagnosis. Early diagnosis and treatment can control the complications and result in better clinical outcomes. | ||
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==Natural History, Complications and Prognosis== | ==Natural History, Complications and Prognosis== | ||
If diabetes mellitus type 2 left untreated, it may result in [[hyperosmolar hyperglycemic state]] (HHS) and in rare circumstances [[diabetic ketoacidosis]] (DKA). These are classified as acute complications of diabetes. Chronic complications of diabetes mellitus include microvascular and macrovascular complications. Early diagnosis and prompt treatment of these complications may result in improved prognosis and less long term morbidity and mortalities.<ref name="pmid27979887">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2017: Summary of Revisions |journal=Diabetes Care |volume=40 |issue=Suppl 1 |pages=S4–S5 |year=2017 |pmid=27979887 |doi=10.2337/dc17-S003 |url=}}</ref> <ref name="pmid7497874">{{cite journal |vauthors=Mogensen CE, Vestbo E, Poulsen PL, Christiansen C, Damsgaard EM, Eiskjaer H, Frøland A, Hansen KW, Nielsen S, Pedersen MM |title=Microalbuminuria and potential confounders. A review and some observations on variability of urinary albumin excretion |journal=Diabetes Care |volume=18 |issue=4 |pages=572–81 |year=1995 |pmid=7497874 |doi= |url=}}</ref><ref name="pmid24145991">{{cite journal |vauthors=Qaseem A, Hopkins RH, Sweet DE, Starkey M, Shekelle P |title=Screening, monitoring, and treatment of stage 1 to 3 chronic kidney disease: A clinical practice guideline from the American College of Physicians |journal=Ann. Intern. Med. |volume=159 |issue=12 |pages=835–47 |year=2013 |pmid=24145991 |doi=10.7326/0003-4819-159-12-201312170-00726 |url=}}</ref><ref name="pmid21115758">{{cite journal |vauthors=Colberg SR, Sigal RJ, Fernhall B, Regensteiner JG, Blissmer BJ, Rubin RR, Chasan-Taber L, Albright AL, Braun B |title=Exercise and type 2 diabetes: the American College of Sports Medicine and the American Diabetes Association: joint position statement |journal=Diabetes Care |volume=33 |issue=12 |pages=e147–67 |year=2010 |pmid=21115758 |pmc=2992225 |doi=10.2337/dc10-9990 |url=}}</ref><ref name="pmid16386666">{{cite journal |vauthors=Scognamiglio R, Negut C, Ramondo A, Tiengo A, Avogaro A |title=Detection of coronary artery disease in asymptomatic patients with type 2 diabetes mellitus |journal=J. Am. Coll. Cardiol. |volume=47 |issue=1 |pages=65–71 |year=2006 |pmid=16386666 |doi=10.1016/j.jacc.2005.10.008 |url=}}</ref><ref name="pmid16757028">{{cite journal |vauthors=Pasquale LR, Kang JH, Manson JE, Willett WC, Rosner BA, Hankinson SE |title=Prospective study of type 2 diabetes mellitus and risk of primary open-angle glaucoma in women |journal=Ophthalmology |volume=113 |issue=7 |pages=1081–6 |year=2006 |pmid=16757028 |doi=10.1016/j.ophtha.2006.01.066 |url=}}</ref> | If diabetes mellitus type 2 left untreated, it may result in [[hyperosmolar hyperglycemic state]] (HHS) and in rare circumstances [[diabetic ketoacidosis]] (DKA). These are classified as acute complications of diabetes. Chronic complications of diabetes mellitus include [[Microvascular disease|microvascular]] and [[Macrovascular disease|macrovascular]] complications. Early diagnosis and prompt treatment of these complications may result in improved prognosis and less long term [[morbidity]] and [[Mortality|mortalities]].<ref name="pmid27979887">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2017: Summary of Revisions |journal=Diabetes Care |volume=40 |issue=Suppl 1 |pages=S4–S5 |year=2017 |pmid=27979887 |doi=10.2337/dc17-S003 |url=}}</ref> <ref name="pmid7497874">{{cite journal |vauthors=Mogensen CE, Vestbo E, Poulsen PL, Christiansen C, Damsgaard EM, Eiskjaer H, Frøland A, Hansen KW, Nielsen S, Pedersen MM |title=Microalbuminuria and potential confounders. A review and some observations on variability of urinary albumin excretion |journal=Diabetes Care |volume=18 |issue=4 |pages=572–81 |year=1995 |pmid=7497874 |doi= |url=}}</ref><ref name="pmid24145991">{{cite journal |vauthors=Qaseem A, Hopkins RH, Sweet DE, Starkey M, Shekelle P |title=Screening, monitoring, and treatment of stage 1 to 3 chronic kidney disease: A clinical practice guideline from the American College of Physicians |journal=Ann. Intern. Med. |volume=159 |issue=12 |pages=835–47 |year=2013 |pmid=24145991 |doi=10.7326/0003-4819-159-12-201312170-00726 |url=}}</ref><ref name="pmid21115758">{{cite journal |vauthors=Colberg SR, Sigal RJ, Fernhall B, Regensteiner JG, Blissmer BJ, Rubin RR, Chasan-Taber L, Albright AL, Braun B |title=Exercise and type 2 diabetes: the American College of Sports Medicine and the American Diabetes Association: joint position statement |journal=Diabetes Care |volume=33 |issue=12 |pages=e147–67 |year=2010 |pmid=21115758 |pmc=2992225 |doi=10.2337/dc10-9990 |url=}}</ref><ref name="pmid16386666">{{cite journal |vauthors=Scognamiglio R, Negut C, Ramondo A, Tiengo A, Avogaro A |title=Detection of coronary artery disease in asymptomatic patients with type 2 diabetes mellitus |journal=J. Am. Coll. Cardiol. |volume=47 |issue=1 |pages=65–71 |year=2006 |pmid=16386666 |doi=10.1016/j.jacc.2005.10.008 |url=}}</ref><ref name="pmid16757028">{{cite journal |vauthors=Pasquale LR, Kang JH, Manson JE, Willett WC, Rosner BA, Hankinson SE |title=Prospective study of type 2 diabetes mellitus and risk of primary open-angle glaucoma in women |journal=Ophthalmology |volume=113 |issue=7 |pages=1081–6 |year=2006 |pmid=16757028 |doi=10.1016/j.ophtha.2006.01.066 |url=}}</ref> | ||
==Diagnosis== | ==Diagnosis== | ||
===History and Symptoms=== | ===History and Symptoms=== | ||
A detailed history must be taken from every person presenting with diabetes symptoms. Classic symptoms of diabetes include: weight loss, polyphagia, polydipsia and polyuria. | A detailed history must be taken from every person presenting with diabetes symptoms. Classic symptoms of diabetes include: [[weight loss]], [[polyphagia]], [[polydipsia]] and [[polyuria]]. Less common symptoms include vision changes, [[tingling]] or [[numbness]] in exterimities, [[fatigue]] and skin changes.<ref name="pmid18519930">{{cite journal |vauthors= |title=Screening for type 2 diabetes mellitus in adults: U.S. Preventive Services Task Force recommendation statement |journal=Ann. Intern. Med. |volume=148 |issue=11 |pages=846–54 |year=2008 |pmid=18519930 |doi= |url=}}</ref><ref name="pmid28070960">{{cite journal |vauthors=Marathe PH, Gao HX, Close KL |title=American Diabetes Association Standards of Medical Care in Diabetes 2017 |journal=J Diabetes |volume=9 |issue=4 |pages=320–324 |year=2017 |pmid=28070960 |doi=10.1111/1753-0407.12524 |url=}}</ref> | ||
===Physical Examination=== | ===Physical Examination=== | ||
Usually patients with diabetes mellitus type 2 have normal physical examination findings unless complications develop in these patients. Common physical examination findings include, pigmented skin patches and acanthosis nigricans. | Usually patients with diabetes mellitus type 2 have normal physical examination findings unless complications develop in these patients. Common physical examination findings include, pigmented skin patches and [[acanthosis nigricans]]. | ||
===Laboratory Findings=== | ===Laboratory Findings=== | ||
Laboratory findings of diabetes mellitus type 2 are diagnostic for this disease. Diabetes may be diagnosed based on plasma glucose criteria, either the fasting plasma glucose (FPG) or the 2-h plasma glucose (2-h PG) value after a 75-g oral glucose tolerance test (OGTT) or A1C criteria. All of these measurements are equally appropriate in diagnosis.<ref name="pmid27979887">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2017: Summary of Revisions |journal=Diabetes Care |volume=40 |issue=Suppl 1 |pages=S4–S5 |year=2017 |pmid=27979887 |doi=10.2337/dc17-S003 |url=}}</ref> | Laboratory findings of diabetes mellitus type 2 are diagnostic for this disease. Diabetes may be diagnosed based on plasma glucose criteria, either the [[fasting plasma glucose]] (FPG) or the 2-h plasma glucose (2-h PG) value after a 75-g [[oral glucose tolerance test]] (OGTT) or [[A1C]] criteria. All of these measurements are equally appropriate in diagnosis.<ref name="pmid27979887">{{cite journal |vauthors= |title=Standards of Medical Care in Diabetes-2017: Summary of Revisions |journal=Diabetes Care |volume=40 |issue=Suppl 1 |pages=S4–S5 |year=2017 |pmid=27979887 |doi=10.2337/dc17-S003 |url=}}</ref> | ||
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|} | |} | ||
==Treatment== | ==Treatment== | ||
Life style modification is fundamental for diabetes management and it's a part of therapy. It include, diabetes self-management education (DSME), diabetes self-management support (DSMS), nutrition therapy, physical activity, smoking cessation counseling, and psychosocial care. The overall objectives of DSME and DSMS are to support informed decision making, self-care behaviors, problem solving, and active collaboration with the health care team to improve clinical outcomes, health status, and quality of life in a cost-effective manner.<ref name="pmid9434653">{{cite journal |vauthors=Kulkarni K, Castle G, Gregory R, Holmes A, Leontos C, Powers M, Snetselaar L, Splett P, Wylie-Rosett J |title=Nutrition Practice Guidelines for Type 1 Diabetes Mellitus positively affect dietitian practices and patient outcomes. The Diabetes Care and Education Dietetic Practice Group |journal=J Am Diet Assoc |volume=98 |issue=1 |pages=62–70; quiz 71–2 |year=1998 |pmid=9434653 |doi= |url=}}</ref><ref name="pmid20536522">{{cite journal |vauthors=Scavone G, Manto A, Pitocco D, Gagliardi L, Caputo S, Mancini L, Zaccardi F, Ghirlanda G |title=Effect of carbohydrate counting and medical nutritional therapy on glycaemic control in Type 1 diabetic subjects: a pilot study |journal=Diabet. Med. |volume=27 |issue=4 |pages=477–9 |year=2010 |pmid=20536522 |doi=10.1111/j.1464-5491.2010.02963.x |url=}}</ref><ref name="pmid20647285">{{cite journal |vauthors=Coppell KJ, Kataoka M, Williams SM, Chisholm AW, Vorgers SM, Mann JI |title=Nutritional intervention in patients with type 2 diabetes who are hyperglycaemic despite optimised drug treatment--Lifestyle Over and Above Drugs in Diabetes (LOADD) study: randomised controlled trial |journal=BMJ |volume=341 |issue= |pages=c3337 |year=2010 |pmid=20647285 |pmc=2907481 |doi= |url=}}</ref><ref name="pmid15220230">{{cite journal |vauthors=Wolf AM, Conaway MR, Crowther JQ, Hazen KY, L Nadler J, Oneida B, Bovbjerg VE |title=Translating lifestyle intervention to practice in obese patients with type 2 diabetes: Improving Control with Activity and Nutrition (ICAN) study |journal=Diabetes Care |volume=27 |issue=7 |pages=1570–6 |year=2004 |pmid=15220230 |doi= |url=}}</ref> | Life style modification is fundamental for diabetes management and it's a part of therapy. It include, diabetes self-management education (DSME), diabetes self-management support (DSMS), nutrition therapy, [[physical activity]], [[smoking cessation]] counseling, and psychosocial care. The overall objectives of DSME and DSMS are to support informed decision making, self-care behaviors, problem solving, and active collaboration with the health care team to improve clinical outcomes, health status, and quality of life in a cost-effective manner.<ref name="pmid9434653">{{cite journal |vauthors=Kulkarni K, Castle G, Gregory R, Holmes A, Leontos C, Powers M, Snetselaar L, Splett P, Wylie-Rosett J |title=Nutrition Practice Guidelines for Type 1 Diabetes Mellitus positively affect dietitian practices and patient outcomes. The Diabetes Care and Education Dietetic Practice Group |journal=J Am Diet Assoc |volume=98 |issue=1 |pages=62–70; quiz 71–2 |year=1998 |pmid=9434653 |doi= |url=}}</ref><ref name="pmid20536522">{{cite journal |vauthors=Scavone G, Manto A, Pitocco D, Gagliardi L, Caputo S, Mancini L, Zaccardi F, Ghirlanda G |title=Effect of carbohydrate counting and medical nutritional therapy on glycaemic control in Type 1 diabetic subjects: a pilot study |journal=Diabet. Med. |volume=27 |issue=4 |pages=477–9 |year=2010 |pmid=20536522 |doi=10.1111/j.1464-5491.2010.02963.x |url=}}</ref><ref name="pmid20647285">{{cite journal |vauthors=Coppell KJ, Kataoka M, Williams SM, Chisholm AW, Vorgers SM, Mann JI |title=Nutritional intervention in patients with type 2 diabetes who are hyperglycaemic despite optimised drug treatment--Lifestyle Over and Above Drugs in Diabetes (LOADD) study: randomised controlled trial |journal=BMJ |volume=341 |issue= |pages=c3337 |year=2010 |pmid=20647285 |pmc=2907481 |doi= |url=}}</ref><ref name="pmid15220230">{{cite journal |vauthors=Wolf AM, Conaway MR, Crowther JQ, Hazen KY, L Nadler J, Oneida B, Bovbjerg VE |title=Translating lifestyle intervention to practice in obese patients with type 2 diabetes: Improving Control with Activity and Nutrition (ICAN) study |journal=Diabetes Care |volume=27 |issue=7 |pages=1570–6 |year=2004 |pmid=15220230 |doi= |url=}}</ref> | ||
===Medical Therapy=== | ===Medical Therapy=== | ||
The main goals of treatment are, eliminate hyperglycemic symptoms, control the long term complications and improve the patient's quality of life. | The main goals of treatment are, eliminate [[hyperglycemic]] symptoms, control the long term complications and improve the patient's quality of life. | ||
Diabetes mellitus type 2 is initially treated by life style modification and weight loss, especially in obese patients. Metformin is the first line pharmacologic therapy that usually starts once the diagnosis is confirmed unless contraindications exist. If glycemic goals does not achieved, the second agent must be add to metformin. A wide range of options are available to add as combination therapy based on patient condition and comorbidities.<br> | Diabetes mellitus type 2 is initially treated by life style modification and [[weight loss]], especially in [[obese]] patients. [[Metformin]] is the first line pharmacologic therapy that usually starts once the diagnosis is confirmed unless contraindications exist. If glycemic goals does not achieved, the second agent must be add to [[metformin]]. A wide range of options are available to add as combination therapy based on patient condition and comorbidities.<br> | ||
Medical therapy starts with metformin monotherapy unless there is a contraindication for it. In following conditions, treatment starts with dual therapy: | Medical therapy starts with [[metformin]] monotherapy unless there is a contraindication for it. In following conditions, treatment starts with dual therapy: | ||
*If HbA1C is greater than 9, start with dual oral blood glucose lowering agent. | *If [[HbA1C]] is greater than 9, start with dual oral blood glucose lowering agent. | ||
*If HbA1C is greater than 10 or blood glucose is more than 300 mg/dl or patient is markedly symptomatic, consider combination therapy with insulin. | *If [[HbA1C]] is greater than 10 or blood glucose is more than 300 mg/dl or patient is markedly symptomatic, consider combination therapy with [[insulin]]. | ||
===Surgery=== | ===Surgery=== | ||
Pancreas and islet cell transplantation is considered in patients with chronic diabetes who have frequent metabolic complications and are intolerant to exogenous insulin or have failed to insulin therapy.<ref name="pmid16567844">{{cite journal |vauthors=Robertson RP, Davis C, Larsen J, Stratta R, Sutherland DE |title=Pancreas and islet transplantation in type 1 diabetes |journal=Diabetes Care |volume=29 |issue=4 |pages=935 |year=2006 |pmid=16567844 |doi= |url=}}</ref> | [[Pancreas transplantation|Pancreas and islet cell transplantation]] is considered in patients with chronic diabetes who have frequent metabolic complications and are intolerant to exogenous [[insulin]] or have failed to [[insulin]] therapy.<ref name="pmid16567844">{{cite journal |vauthors=Robertson RP, Davis C, Larsen J, Stratta R, Sutherland DE |title=Pancreas and islet transplantation in type 1 diabetes |journal=Diabetes Care |volume=29 |issue=4 |pages=935 |year=2006 |pmid=16567844 |doi= |url=}}</ref> | ||
===Primary Prevention=== | ===Primary Prevention=== | ||
Life style modification is the main stay for diabetes mellitus prevention. Metformin is another adjunctive measure to prevent diabetes in high risk persons. Studies have shown that 7% [[weight loss]] during 6 months is effective for diabetes prevention.<ref name="pmid17098085">{{cite journal |vauthors=Lindström J, Ilanne-Parikka P, Peltonen M, Aunola S, Eriksson JG, Hemiö K, Hämäläinen H, Härkönen P, Keinänen-Kiukaanniemi S, Laakso M, Louheranta A, Mannelin M, Paturi M, Sundvall J, Valle TT, Uusitupa M, Tuomilehto J |title=Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study |journal=Lancet |volume=368 |issue=9548 |pages=1673–9 |year=2006 |pmid=17098085 |doi=10.1016/S0140-6736(06)69701-8 |url=}}</ref> | Life style modification is the main stay for diabetes mellitus prevention. [[Metformin]] is another adjunctive measure to prevent diabetes in high risk persons. Studies have shown that 7% [[weight loss]] during 6 months is effective for diabetes prevention.<ref name="pmid17098085">{{cite journal |vauthors=Lindström J, Ilanne-Parikka P, Peltonen M, Aunola S, Eriksson JG, Hemiö K, Hämäläinen H, Härkönen P, Keinänen-Kiukaanniemi S, Laakso M, Louheranta A, Mannelin M, Paturi M, Sundvall J, Valle TT, Uusitupa M, Tuomilehto J |title=Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study |journal=Lancet |volume=368 |issue=9548 |pages=1673–9 |year=2006 |pmid=17098085 |doi=10.1016/S0140-6736(06)69701-8 |url=}}</ref> | ||
===Secondary Prevention=== | ===Secondary Prevention=== | ||
The most important aspect of secondary prevention in diabetes mellitus type 2 is, to decrease the macrovascular mortality. Among the preventive measures, lipid control, smoking cessation and hypertension treatment are the most important ones. | The most important aspect of secondary prevention in diabetes mellitus type 2 is, to decrease the macrovascular mortality. Among the preventive measures, [[lipid]] control, [[smoking cessation]] and [[hypertension]] treatment are the most important ones. | ||
==References== | ==References== | ||
Revision as of 19:25, 22 March 2017
|
Diabetes mellitus type 2 Microchapters |
|
Differentiating Diabetes Mellitus Type 2 from other Diseases |
|
Diagnosis |
|
Treatment |
|
Medical therapy |
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]; Tarek Nafee, M.D. [4],Seyedmahdi Pahlavani, M.D. [5]
Overview
Diabetes mellitus type 2 (formerly called non insulin-dependent diabetes (NIDDM), obesity related diabetes, or adult-onset diabetes) is a metabolic disorder that is primarily characterized by insulin resistance, relative insulin deficiency, and hyperglycemia. The defective responsiveness of body tissues to insulin almost certainly involves the insulin receptor in cell membranes. In the early stage the predominant abnormality is reduced insulin sensitivity, characterized by elevated levels of insulin in the blood. At this stage hyperglycemia can be managed by engaging in exercise, modifying one's diet and medications that improve insulin sensitivity or reduce glucose production by the liver. As the disease progresses the impairment of insulin secretion worsens, and therapeutic replacement of insulin often becomes necessary. It is rapidly increasing in the developed world, and there is some evidence that this pattern will be followed in much of the rest of the world in coming years. The CDC has characterized the increase as an epidemic.[1]
Historical Perspective
Diabetes mellitus is a well-recognized disease from ancient times. In 1812 diabetes mellitus became a recognized clinical entity in The New England Journal of Medicine and Surgery. In 1889, the pancreas was identified as playing a major role in the pathogenesis of the disease. The discovery of insulin in 1921 was a major turning point in the history of diabetes when Frederick Banting and Charles Best were able to reverse the diabetic state in dogs by injecting pancreatic isolate from healthy dogs.
Classification
Diabetes is classified in to 3 main categories.
Pathophysiology
The underlying pathology is the development of insulin resistance. Contrary to type 1 diabetes, patients with type 2 diabetes sufficiently produce insulin; however, cellular response to the circulating insulin is diminished. The mechanism by which the insulin resistance develops is postulated to be influenced by both genetic and environmental factors. Environmental influences on the pathogenesis of type 2 DM include high glycemic diets, central obesity, older age, male gender, low-fiber diet, and high saturated fat diet.
Causes
The underlying cause of type 2 diabetes is insulin resistance. The exact cacuse of insulin resistance is not known, however several theories exist. Central obesity, aging, and high glycemic diets are most commonly implicated in the development of type 2 diabetes.
Differentiating Diabetes mellitus type 2 from other Diseases
Type 2 diabetes mellitus must be differentiated from other disorders that may present with polyuria, polydipsia, weight loss or weight gain. Such disorders may include other forms of diabetes mellitus (e.g. type 1 DM, MODY) or other endocrine disorders (e.g. hypothyroidism, cushings syndrome, wolfram syndrome, alstrom syndrome) or drug that can cause hyperglycemia (e.g. glucocorticoids)
Epidemiology and Demographics
The prevalence of type 2 diabetes mellitus (DM) is well studied in the United States and other developed countries. However, worldwide there is a large variation in the results of the population studies in developing countries and particularly in rural areas with poor access to healthcare. For this reason, diabetes is estimated to be undiagnosed in approximately 50% of adults worldwide. In the United States, African Americans, Mexican Americans, American Indians and non-Hispanic blacks are at a higher risk of developing type 2 diabetes compared to non-Hispanic whites. It is more prevalent among those older than 65 years, although there is a growing tend of childhood-onset of the disease. In 2011, 335 million people were estimated to have type 2 diabetes and that number is on a trajectory to reach over 500 million people by 2050. These figures correlate with a prevalence of approximately 5000 and 7500 per 100,000 in 2011 and 2050, respectively. Type 2 diabetes is more prevalent among men than women and in countries with low to mid income levels compared to high income level countries. It is classified as a global epidemic that is growing in parallel to massive urbanization.[2] [3]
Risk Factors
Common risk factors associated with development of type 2 diabetes include: positive family history, certain ethnicity, obesity, smoking, physical inactivity, poor dietary habits, certain drugs (.eg. glucocorticoids) and certain medical conditions that may result in weight gain and inactivity.[4][5][6][7][8][9][10][11][12][13]
Screening
Diabetes screening is recommended for many people at various stages of life, and for those with any of several risk factors. Screening tests are the same tests used for diagnosis. Early diagnosis and treatment can control the complications and result in better clinical outcomes.
| Criteria for testing for diabetes or prediabetes in asymptomatic adults |
|---|
Testing should be considered in overweight or obese (BMI ≥25 kg/m2 or ≥23 kg/m2 in Asian Americans) adults who have one or more of the following risk factors:
|
| For all patients, testing should begin at age 45 years. |
| If results are normal, testing should be repeated at a minimum of 3-year intervals, with consideration of more frequent testing depending on initial results (e.g., those with
prediabetes should be tested yearly) and risk status. |
Natural History, Complications and Prognosis
If diabetes mellitus type 2 left untreated, it may result in hyperosmolar hyperglycemic state (HHS) and in rare circumstances diabetic ketoacidosis (DKA). These are classified as acute complications of diabetes. Chronic complications of diabetes mellitus include microvascular and macrovascular complications. Early diagnosis and prompt treatment of these complications may result in improved prognosis and less long term morbidity and mortalities.[14] [15][16][17][18][19]
Diagnosis
History and Symptoms
A detailed history must be taken from every person presenting with diabetes symptoms. Classic symptoms of diabetes include: weight loss, polyphagia, polydipsia and polyuria. Less common symptoms include vision changes, tingling or numbness in exterimities, fatigue and skin changes.[20][21]
Physical Examination
Usually patients with diabetes mellitus type 2 have normal physical examination findings unless complications develop in these patients. Common physical examination findings include, pigmented skin patches and acanthosis nigricans.
Laboratory Findings
Laboratory findings of diabetes mellitus type 2 are diagnostic for this disease. Diabetes may be diagnosed based on plasma glucose criteria, either the fasting plasma glucose (FPG) or the 2-h plasma glucose (2-h PG) value after a 75-g oral glucose tolerance test (OGTT) or A1C criteria. All of these measurements are equally appropriate in diagnosis.[14]
| Criteria for the diagnosis of diabetes |
|---|
| FPG ≥126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8 h. |
| OR |
| 2-h Plasma Glucose (PG) ≥200 mg/dL (11.1 mmol/L) during an OGTT. The test should be performed as described
by the WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water. |
| OR |
| A1C ≥6.5% (48 mmol/mol). |
| OR |
| In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL (11.1 mmol/L). |
Treatment
Life style modification is fundamental for diabetes management and it's a part of therapy. It include, diabetes self-management education (DSME), diabetes self-management support (DSMS), nutrition therapy, physical activity, smoking cessation counseling, and psychosocial care. The overall objectives of DSME and DSMS are to support informed decision making, self-care behaviors, problem solving, and active collaboration with the health care team to improve clinical outcomes, health status, and quality of life in a cost-effective manner.[22][23][24][25]
Medical Therapy
The main goals of treatment are, eliminate hyperglycemic symptoms, control the long term complications and improve the patient's quality of life.
Diabetes mellitus type 2 is initially treated by life style modification and weight loss, especially in obese patients. Metformin is the first line pharmacologic therapy that usually starts once the diagnosis is confirmed unless contraindications exist. If glycemic goals does not achieved, the second agent must be add to metformin. A wide range of options are available to add as combination therapy based on patient condition and comorbidities.
Medical therapy starts with metformin monotherapy unless there is a contraindication for it. In following conditions, treatment starts with dual therapy:
- If HbA1C is greater than 9, start with dual oral blood glucose lowering agent.
- If HbA1C is greater than 10 or blood glucose is more than 300 mg/dl or patient is markedly symptomatic, consider combination therapy with insulin.
Surgery
Pancreas and islet cell transplantation is considered in patients with chronic diabetes who have frequent metabolic complications and are intolerant to exogenous insulin or have failed to insulin therapy.[26]
Primary Prevention
Life style modification is the main stay for diabetes mellitus prevention. Metformin is another adjunctive measure to prevent diabetes in high risk persons. Studies have shown that 7% weight loss during 6 months is effective for diabetes prevention.[27]
Secondary Prevention
The most important aspect of secondary prevention in diabetes mellitus type 2 is, to decrease the macrovascular mortality. Among the preventive measures, lipid control, smoking cessation and hypertension treatment are the most important ones.
References
- ↑ Gerberding, Julie Louise (2007-05-24), Diabetes, Disabling Disease to Double by 2050, CDC
- ↑ GBD 2015 Disease and Injury Incidence and Prevalence Collaborators (2016). "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1545–1602. doi:10.1016/S0140-6736(16)31678-6. PMC 5055577. PMID 27733282.
- ↑ "IDF Diabetes Atlas 7th Edition". IDF. Brussels, Belgium: International Diabetes Federation. 2015. Retrieved 9 March 2017.
- ↑ Scott RA, Langenberg C, Sharp SJ, Franks PW, Rolandsson O, Drogan D, van der Schouw YT, Ekelund U, Kerrison ND, Ardanaz E, Arriola L, Balkau B, Barricarte A, Barroso I, Bendinelli B, Beulens JW, Boeing H, de Lauzon-Guillain B, Deloukas P, Fagherazzi G, Gonzalez C, Griffin SJ, Groop LC, Halkjaer J, Huerta JM, Kaaks R, Khaw KT, Krogh V, Nilsson PM, Norat T, Overvad K, Panico S, Rodriguez-Suarez L, Romaguera D, Romieu I, Sacerdote C, Sánchez MJ, Spijkerman AM, Teucher B, Tjonneland A, Tumino R, van der A DL, Wark PA, McCarthy MI, Riboli E, Wareham NJ (2013). "The link between family history and risk of type 2 diabetes is not explained by anthropometric, lifestyle or genetic risk factors: the EPIC-InterAct study". Diabetologia. 56 (1): 60–9. doi:10.1007/s00125-012-2715-x. PMC 4038917. PMID 23052052.
- ↑ Meigs JB, Cupples LA, Wilson PW (2000). "Parental transmission of type 2 diabetes: the Framingham Offspring Study". Diabetes. 49 (12): 2201–7. PMID 11118026.
- ↑ Mokdad AH, Ford ES, Bowman BA, Dietz WH, Vinicor F, Bales VS, Marks JS (2003). "Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001". JAMA. 289 (1): 76–9. PMID 12503980.
- ↑ Nguyen NT, Nguyen XM, Lane J, Wang P (2011). "Relationship between obesity and diabetes in a US adult population: findings from the National Health and Nutrition Examination Survey, 1999-2006". Obes Surg. 21 (3): 351–5. doi:10.1007/s11695-010-0335-4. PMC 3040808. PMID 21128002.
- ↑ Friedman JE, Dohm GL, Leggett-Frazier N, Elton CW, Tapscott EB, Pories WP, Caro JF (1992). "Restoration of insulin responsiveness in skeletal muscle of morbidly obese patients after weight loss. Effect on muscle glucose transport and glucose transporter GLUT4". J. Clin. Invest. 89 (2): 701–5. doi:10.1172/JCI115638. PMC 442905. PMID 1737857.
- ↑ Chan JM, Rimm EB, Colditz GA, Stampfer MJ, Willett WC (1994). "Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men". Diabetes Care. 17 (9): 961–9. PMID 7988316.
- ↑ Manson JE, Ajani UA, Liu S, Nathan DM, Hennekens CH (2000). "A prospective study of cigarette smoking and the incidence of diabetes mellitus among US male physicians". Am. J. Med. 109 (7): 538–42. PMID 11063954.
- ↑ Feskens EJ, Kromhout D (1989). "Cardiovascular risk factors and the 25-year incidence of diabetes mellitus in middle-aged men. The Zutphen Study". Am. J. Epidemiol. 130 (6): 1101–8. PMID 2589303.
- ↑ Rimm EB, Chan J, Stampfer MJ, Colditz GA, Willett WC (1995). "Prospective study of cigarette smoking, alcohol use, and the risk of diabetes in men". BMJ. 310 (6979): 555–9. PMC 2548937. PMID 7888928.
- ↑ Foy CG, Bell RA, Farmer DF, Goff DC, Wagenknecht LE (2005). "Smoking and incidence of diabetes among U.S. adults: findings from the Insulin Resistance Atherosclerosis Study". Diabetes Care. 28 (10): 2501–7. PMID 16186287.
- ↑ 14.0 14.1 "Standards of Medical Care in Diabetes-2017: Summary of Revisions". Diabetes Care. 40 (Suppl 1): S4–S5. 2017. doi:10.2337/dc17-S003. PMID 27979887.
- ↑ Mogensen CE, Vestbo E, Poulsen PL, Christiansen C, Damsgaard EM, Eiskjaer H, Frøland A, Hansen KW, Nielsen S, Pedersen MM (1995). "Microalbuminuria and potential confounders. A review and some observations on variability of urinary albumin excretion". Diabetes Care. 18 (4): 572–81. PMID 7497874.
- ↑ Qaseem A, Hopkins RH, Sweet DE, Starkey M, Shekelle P (2013). "Screening, monitoring, and treatment of stage 1 to 3 chronic kidney disease: A clinical practice guideline from the American College of Physicians". Ann. Intern. Med. 159 (12): 835–47. doi:10.7326/0003-4819-159-12-201312170-00726. PMID 24145991.
- ↑ Colberg SR, Sigal RJ, Fernhall B, Regensteiner JG, Blissmer BJ, Rubin RR, Chasan-Taber L, Albright AL, Braun B (2010). "Exercise and type 2 diabetes: the American College of Sports Medicine and the American Diabetes Association: joint position statement". Diabetes Care. 33 (12): e147–67. doi:10.2337/dc10-9990. PMC 2992225. PMID 21115758.
- ↑ Scognamiglio R, Negut C, Ramondo A, Tiengo A, Avogaro A (2006). "Detection of coronary artery disease in asymptomatic patients with type 2 diabetes mellitus". J. Am. Coll. Cardiol. 47 (1): 65–71. doi:10.1016/j.jacc.2005.10.008. PMID 16386666.
- ↑ Pasquale LR, Kang JH, Manson JE, Willett WC, Rosner BA, Hankinson SE (2006). "Prospective study of type 2 diabetes mellitus and risk of primary open-angle glaucoma in women". Ophthalmology. 113 (7): 1081–6. doi:10.1016/j.ophtha.2006.01.066. PMID 16757028.
- ↑ "Screening for type 2 diabetes mellitus in adults: U.S. Preventive Services Task Force recommendation statement". Ann. Intern. Med. 148 (11): 846–54. 2008. PMID 18519930.
- ↑ Marathe PH, Gao HX, Close KL (2017). "American Diabetes Association Standards of Medical Care in Diabetes 2017". J Diabetes. 9 (4): 320–324. doi:10.1111/1753-0407.12524. PMID 28070960.
- ↑ Kulkarni K, Castle G, Gregory R, Holmes A, Leontos C, Powers M, Snetselaar L, Splett P, Wylie-Rosett J (1998). "Nutrition Practice Guidelines for Type 1 Diabetes Mellitus positively affect dietitian practices and patient outcomes. The Diabetes Care and Education Dietetic Practice Group". J Am Diet Assoc. 98 (1): 62–70, quiz 71–2. PMID 9434653.
- ↑ Scavone G, Manto A, Pitocco D, Gagliardi L, Caputo S, Mancini L, Zaccardi F, Ghirlanda G (2010). "Effect of carbohydrate counting and medical nutritional therapy on glycaemic control in Type 1 diabetic subjects: a pilot study". Diabet. Med. 27 (4): 477–9. doi:10.1111/j.1464-5491.2010.02963.x. PMID 20536522.
- ↑ Coppell KJ, Kataoka M, Williams SM, Chisholm AW, Vorgers SM, Mann JI (2010). "Nutritional intervention in patients with type 2 diabetes who are hyperglycaemic despite optimised drug treatment--Lifestyle Over and Above Drugs in Diabetes (LOADD) study: randomised controlled trial". BMJ. 341: c3337. PMC 2907481. PMID 20647285.
- ↑ Wolf AM, Conaway MR, Crowther JQ, Hazen KY, L Nadler J, Oneida B, Bovbjerg VE (2004). "Translating lifestyle intervention to practice in obese patients with type 2 diabetes: Improving Control with Activity and Nutrition (ICAN) study". Diabetes Care. 27 (7): 1570–6. PMID 15220230.
- ↑ Robertson RP, Davis C, Larsen J, Stratta R, Sutherland DE (2006). "Pancreas and islet transplantation in type 1 diabetes". Diabetes Care. 29 (4): 935. PMID 16567844.
- ↑ Lindström J, Ilanne-Parikka P, Peltonen M, Aunola S, Eriksson JG, Hemiö K, Hämäläinen H, Härkönen P, Keinänen-Kiukaanniemi S, Laakso M, Louheranta A, Mannelin M, Paturi M, Sundvall J, Valle TT, Uusitupa M, Tuomilehto J (2006). "Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study". Lancet. 368 (9548): 1673–9. doi:10.1016/S0140-6736(06)69701-8. PMID 17098085.