- Diabetes mellitus type 2
Diabetes mellitus type 2 Classification and external resources
Universal blue circle symbol for diabetes.
ICD-10 E11 ICD-9 250.00, 250.02 OMIM 125853 DiseasesDB 3661 MedlinePlus 000313 eMedicine article/117853 MeSH D003924
Diabetes mellitus type 2 – formerly non-insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes – is a metabolic disorder that is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency. Diabetes is often initially managed by increasing exercise and dietary modification. If the condition progresses, medications may be needed. Often affecting the obese, diabetes requires patients to routinely check their blood sugar.
Unlike type 1 diabetes, there is very little tendency toward ketoacidosis although it is not unheard of. One effect that can occur is nonketonic hyperglycemia. Long-term complications from high blood sugar can include increased risk of heart attacks, strokes, diabetic retinopathy where eye sight is affected, and kidney failure. For extreme cases, circulation of limbs is affected, potentially requiring amputation. Loss of hearing, eyesight, and cognitive ability has also been linked to this condition.
Signs and symptoms
The classic symptoms of diabetes are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), fatigue and weight loss. Type II diabetes has been associated with an increased risk of cognitive dysfunction and dementia through disease processes such as Alzheimer's disease and vascular dementia. Researchers have shown that reduced glucose tolerance has deleterious effects on memory in the elderly, and concomitant hippocampal atrophy.
Type 2 diabetes is due to a combination of lifestyle and genetic factors. Recently, intrauterine growth restriction (IUGR) or prenatal undernutrition (macro- and micronutrient) was identified as another probable factor  A clue for this concept was the Dutch Hunger Winter (1944-1945) during World War II, and the pioneering work of Professor Barker.
A number of lifestyle factors are known to be important to the development of type 2 diabetes. In one study, those who had high levels of physical activity, a healthy diet, did not smoke, and consumed alcohol in moderation had an 82% lower rate of diabetes. When a normal weight was included, the rate was 89% lower. In this study, a healthy diet was defined as one high in fiber, with a high polyunsaturated to saturated fat ratio, and a lower mean glycemic index. Obesity has been found to contribute to approximately 55% of cases of type 2 diabetes, and decreasing consumption of saturated fats and trans fatty acids while replacing them with unsaturated fats may decrease the risk. The increased rate of childhood obesity between the 1960s and 2000s is believed to have led to the increase in type 2 diabetes in children and adolescents. Dietary fat intake is linked to diabetes risk.
A 2010 meta-analysis of eleven studies involving 310,819 participants and 15,043 cases of type 2 diabetes found that "SSBs [sugar-sweetened beverages] may increase the risk of metabolic syndrome and type 2 diabetes not only through obesity but also by increasing dietary glycemic load, leading to insulin resistance, β-cell dysfunction, and inflammation."
Environmental toxins may contribute to recent increases in the rate of type 2 diabetes. A weak positive correlation has been found between the concentration in the urine of bisphenol A, a constituent of some plastics, and the incidence of type 2 diabetes.
There are many factors which can potentially give rise to, or exacerbate, type 2 diabetes. These include obesity, hypertension, elevated cholesterol (combined hyperlipidemia), and with the condition often termed metabolic syndrome (it is also known as Syndrome X, Reavan's syndrome, or CHAOS). Other causes include acromegaly, Cushing's syndrome, thyrotoxicosis, pheochromocytoma, chronic pancreatitis, cancer, and drugs. Additional factors found to increase the risk of type 2 diabetes include aging, high-fat diets and a less active lifestyle.
Subclinical Cushing's syndrome (cortisol excess) may be associated with type 1 diabetes. The percentage of subclinical Cushing's syndrome in the diabetic population is about 9%. Diabetic patients with a pituitary microadenoma can improve insulin sensitivity by removal of these microadenomas.
Hypogonadism is often associated with cortisol excess, and testosterone deficiency is also associated with type 2 diabetes, even if the exact mechanism by which testosterone improves insulin sensitivity is still not known.
There is also a strong inheritable genetic connection in type 2 diabetes: having relatives (especially first degree) with type 2 increases risks of developing type 2 diabetes substantially. Genetic risk for type 2 diabetes decreased as humans first began migrating around the world, implying a strong environmental component has affected the genetic-basis of 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.
About 55 percent of type 2 diabetes patients are obese at diagnosis —chronic obesity leads to increased insulin resistance that can develop into type 2 diabetes, most likely because adipose tissue (especially that in the abdomen around internal organs) is a source of several chemical signals, hormones and cytokines, to other tissues. Inflammatory cytokines for example may activate the NF-κB pathway which has been linked to the development of insulin resistance.
Other research shows that type 2 diabetes causes obesity as an effect of the changes in metabolism and other deranged cell behavior attendant on insulin resistance.
However, environmental factors (almost certainly diet and weight) play a large part in the development of type 2 diabetes in addition to any genetic component. This can be seen from the adoption of the type 2 diabetes epidemiological pattern in those who have moved to a different environment as compared to the same genetic pool who have not. Immigrants to Western developed countries, for instance, as compared to lower incidence countries of origins. Such developments can also be found in environments which have had a recent increase in social wealth, increasingly common throughout Asia.
There is a stronger inheritance pattern for type 2 diabetes. Those with first-degree relatives with type 2 diabetes have a much higher risk of developing type 2 diabetes, increasing with the number of those relatives. Concordance among monozygotic twins is close to 100%, and about 25% of those with the disease have a family history of diabetes. Genes significantly associated with developing type 2 diabetes, include TCF7L2, PPARG, FTO, KCNJ11, NOTCH2, WFS1, CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX. KCNJ11 (potassium inwardly rectifying channel, subfamily J, member 11), encodes the islet ATP-sensitive potassium channel Kir6.2, and TCF7L2 (transcription factor 7–like 2) regulates proglucagon gene expression and thus the production of glucagon-like peptide-1. Moreover, obesity (which is an independent risk factor for type 2 diabetes) is strongly inherited.
Various hereditary conditions may feature diabetes, for example myotonic dystrophy and Friedreich's ataxia. Wolfram's syndrome is an autosomal recessive neurodegenerative disorder that first becomes evident in childhood. It consists of diabetes insipidus, diabetes mellitus, optic atrophy, and deafness, hence the acronym DIDMOAD.
Gene expression promoted by a diet of fat and glucose, as well as high levels of inflammation related cytokines found in the obese, results in cells that "produce fewer and smaller mitochondria than is normal," and are thus prone to insulin resistance.
This is a more complex problem than type 1, but is sometimes easier to treat, especially in the early years when insulin is often still being produced internally. Severe complications can result from improperly managed type 2 diabetes, including renal failure, erectile dysfunction, blindness, slow healing wounds (including surgical incisions), and arterial disease, including coronary artery disease. The onset of type 2 diabetes has been most common in middle age and later life, although it is being more frequently seen in adolescents and young adults due to an increase in child obesity and inactivity. A type of diabetes called MODY is increasingly seen in adolescents, but this is classified as a diabetes due to a specific cause and not as type 2 diabetes.
In the 2008 Banting Lecture of the American Diabetes Association, DeFronzo enumerates eight main pathophysiological factors in the type 2 diabetic organism 
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 or diabetes due to a specific cause. Examples include diabetes mellitus such as MODY or those caused by hemochromatosis, pancreatic insufficiencies, or certain types of medications (e.g., long-term steroid use).
Recent studies of pancreatic beta cells have indicated a molecular connection between diet, obesity that involves the role of fat in activating a pathway to type 2 diabetes. In this mechanism, loss of beta cell glucose sensing contributes substantially to the early manifestation of diabetes, and beta cell dysfunction is responsible for the onset and severity of multiple systemic disease signs including impaired glucose tolerance, hyperglycemia, hepatic steatosis and insulin resistance in muscle and adipose cells. Previous work published in past decades by the laboratories of Roger Unger, Jerrold Olefsky, and Bernard Thorens alluded to the possibility of the importance of beta cell function and glucose sensing in these disease signs. This mechanism of beta cell dysfunction may be contributing substantially to the current epidemic of type 2 diabetes.
2006 WHO Diabetes criteria Condition 2 hour glucose Fasting glucose mmol/l(mg/dl) mmol/l(mg/dl) Normal <7.8 (<140) <6.1 (<110) Impaired fasting glycaemia <7.8 (<140) ≥ 6.1(≥110) & <7.0(<126) Impaired glucose tolerance ≥7.8 (≥140) <7.0 (<126) Diabetes mellitus ≥11.1 (≥200) ≥7.0 (≥126)
The World Health Organization definition of diabetes is for a single raised glucose reading with symptoms, otherwise raised values on two occasions, of either:
- fasting plasma glucose ≥ 7.0 mmol/l (126 mg/dl)
- With a glucose tolerance test, two hours after the oral dose a plasma glucose ≥ 11.1 mmol/l (200 mg/dl)
If a 2-hour postload glucose level of at least 11.1 mmol/L (≥ 200 mg/dL) is used as the reference standard, the fasting plasma glucose > 7.0 mmol/L (126 mg/dL) diagnoses current diabetes with:
- sensitivity about 50%
- specificity greater than 95%
A random capillary blood glucose > 6.7 mmol/L (120 mg/dL) diagnoses current diabetes with:
- sensitivity = 75%
- specificity = 88%
Glycated hemoglobin values that are elevated (over 5%), but not in the diabetic range (not over 7.0%) are predictive of subsequent clinical diabetes in United States female health professionals. In this study, 177 of 1061 patients with glycated hemoglobin value less than 6% became diabetic within 5 years compared to 282 of 26281 patients with a glycated hemoglobin value of 6.0% or more. This equates to a glycated hemoglobin value of 6.0% or more having:
- sensitivity = 16.7%
- specificity = 98.9%
No major organization recommends universal screening for diabetes as there is no evidence that such a program would improve outcomes. Screening is recommended by the United States Preventive Services Task Force in adults without symptoms whose blood pressure is greater than 135/80 mmHg. For those whose blood pressure is less, the evidence is insufficient to recommend for or against screening. The World Health Organization recommends only testing those groups at high risk. Based on a survey conducted in 2011 on 70,000 average persons, the Hungarian Diabetes Society recommends the introduction of a general screening of the adult population for Diabetes Type II.
Onset of type 2 diabetes can be delayed or prevented through proper nutrition and regular exercise. Intensive lifestyle measures may reduce the risk by over half. Evidence for the benefit of dietary changes alone however is limited. In those with impaired glucose tolerance, diet and exercise and/or metformin or acarbose may decrease the risk of developing diabetes. Lifestyle interventions are more effective than metformin.
Management of type 2 diabetes focuses on lifestyle interventions, lowering other cardiovascular risk factors, and maintaining blood glucose levels in the normal range. Self-monitoring of blood glucose for people with newly diagnosed type 2 diabetes was recommended by the National Health Services in 2008 however the benefit of self monitoring in those not using multi-dose insulin is questionable. Managing other cardiovascular risk factors including hypertension, high cholesterol, and microalbuminuria improves a person's life expectancy. Intensive blood sugar lowering as opposed to standard blood sugar lowering does not appear to change mortality.
Aerobic exercise is beneficial in diabetes with a greater amount of exercise yielding better results. It leads to a decrease in HbA1C, improved insulin sensitivity, and a better V02 max. Resistance training is also useful and the combination of both types of exercise may be most effective. A diabetic diet that promotes weight loss is important. While the best diet type to achieve this is controversial a low glycemic index diet has been found to improve blood sugar control. Culturally appropriate education may help people with type 2 diabetes control their blood sugar levels, for up to six months at least.
There are several classes of medications available. Metformin is generally recommended as a first line treatment as there is good evidence that it decreases mortality. Injections of insulin may either be added to oral medication or used alone. Other classes of medications used to treat type 2 diabetes are sulfonylureas, nonsulfonylurea secretagogues, alpha glucosidase inhibitors, and thiazolidinediones.
The initial insulin regimen is often chosen based on the patient's blood glucose profile. Initially, adding nightly insulin to patients failing oral medications may be best. Nightly insulin combines better with metformin than with sulfonylureas.
When nightly insulin is insufficient, choices include:
- Premixed insulin with a fixed ratio of short and intermediate acting insulin; this tends to be more effective than long acting insulin, but is associated with increased hypoglycemia. Initial total daily dosage of biphasic insulin can be 10 units if the fasting plasma glucose values are less than 180 mg/dl or 12 units when the fasting plasma glucose is above 180 mg/dl". A guide to titrating fixed ratio insulin is available.
- Long acting insulins include insulin glargine and insulin detemir. A meta-analysis of randomized controlled trials by the Cochrane Collaboration found "only a minor clinical benefit of treatment with long-acting insulin analogues for patients with diabetes mellitus type 2". More recently, a randomized controlled trial found that although long acting insulins were less effective, they were associated with reduced hypoglycemic episodes.
Gastric Bypass procedures are currently considered an elective procedure with no universally accepted algorithm to decide who should have the surgery. In the diabetic patient, certain types result in 99-100% prevention of insulin resistance and 80-90% clinical resolution or remission of type 2 diabetes. In 1991, the NIH (National Institutes of Health) Consensus Development Conference on Gastrointestinal Surgery for Obesity proposed that the body mass index (BMI) threshold to consider surgery should drop from 40 to 35 in the appropriate patient. More recently, the American Society for Bariatric Surgery (ASBS) and the ASBS Foundation suggested that the BMI threshold be lowered to 30 in the presence of severe co-morbidities. Debate has flourished about the role of gastric bypass surgery in type 2 diabetics since the publication of The Swedish Obese Subjects Study. The largest prospective series showed a large decrease in the occurrence of type 2 diabetes in the post-gastric bypass patient at both 2 years (odds ratio was 0.14) and at 10 years (odds ratio was 0.25).
A study of 20-years of Greenville (US) gastric bypass patients found that 80% of those with type 2 diabetes before surgery no longer required insulin or oral agents to maintain normal glucose levels. Weight loss occurred rapidly in many people in the study who had had the surgery. The 20% who did not respond to bypass surgery were, typically, those who were older and had had diabetes for over 20 years.
The way type 2 diabetes is managed may change with age. Insulin production decreases because of age-related impairment of pancreatic beta cells. Additionally, insulin resistance increases because of the loss of lean tissue and the accumulation of fat, particularly intra-abdominal fat, and the decreased tissue sensitivity to insulin. Glucose tolerance progressively declines with age, leading to a high prevalence of type 2 diabetes and postchallenge hyperglycemia in the older population. Age-related glucose intolerance is often accompanied by insulin resistance, but circulating insulin levels are similar to those of younger people. Treatment goals for older patients with diabetes vary with the individual, and take into account health status, as well as life expectancy, level of dependence, and willingness to adhere to a treatment regimen.
Even if properly and carefully managed, type 2 diabetes is currently a chronic disease, which is, in most cases, compatible with an otherwise full life. Some cases, for reasons obscure, cannot be reasonably managed and lead to damage or even death sooner than later. Non-compliance with management is a contributor in some cases (unwillingness to monitor blood glucose, take prescribed medication, or reliance on unusual or exotic treatment regimes without credible track record), but not all. Much of the damage is due to the complications of diabetes, not directly to diabetes' acute effects. For example, in the developed world, and increasingly elsewhere, type 2 diabetes is the largest cause of non-traumatic blindness and kidney failure.
Research continues and several potential treatments may result in "cures". Examples include resection surgery of the upper small intestine, and very stringent restricted calorie diets. None is, as of 2011, sufficiently well understood, or adequately tested, to be of clinical significance. One or more might, possibly, become clinically significant for some cases, or even all, but this is some years away in the most fortunate instance.
Globally in 2003 it was estimated that there were 150 million people with type 2 diabetes. The incidence varies substantially in different parts of the world, almost certainly because of environmental and lifestyle factors, though these are not known in detail. In the United States there are 23.6 million people (7.8% of the population) with diabetes with 17.9 million being diagnosed, 90% of whom are type 2. With prevalence rates doubling between 1990 and 2005, CDC has characterized the increase as an epidemic. Traditionally considered a disease of adults, type 2 diabetes is increasingly diagnosed in children in parallel to rising obesity rates  due to alterations in dietary patterns as well as in life styles during childhood.
Type-2 diabetes mellitus is known to affect ethnic subgroups differently due to unique risk factors. For example, African Americans have a 12-fold greater prevalence than black natives of Africa.  Cross-sectional epidemiological data suggests that the population with the highest type-two diabetes prevalence, however is the American Pima Indians.  Their prevalence rates of 38% are substantially higher than those of Pima Indians in Mexico (prevalence of 6.9%). It appears that both insulin resistance and beta-cell dysfunction were common, leading to inherent genetic predisposition to type-2 diabetes across all Pima Indians. It is therefore concluded that the disproportionately high prevalence of diabetes in American Pima Indians is likely due to changes in westernization and urbanization of lifestyle/ environmental conditions in conjunction with underlying physiological predisposition.
- ^ "Diabetes Blue Circle Symbol". International Diabetes Federation. 17 March 2006. http://www.diabetesbluecircle.org.
- ^ 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. 1194–1195. ISBN 0-7216-0187-1.
- ^ Fasanmade, OA; Odeniyi, IA, Ogbera, AO (2008 Jun). "Diabetic ketoacidosis: diagnosis and management.". African journal of medicine and medical sciences 37 (2): 99–105. PMID 18939392.
- ^ Cooke DW, Plotnick L (November 2008). "Type 1 diabetes mellitus in pediatrics". Pediatr Rev 29 (11): 374–84; quiz 385. doi:10.1542/pir.29-11-374. PMID 18977856.
- ^ Convit A, Wolf OT, Tarshish C, de Leon MJ. Reduced glucose tolerance is associated with poor memory performance and hippocampal atrophy among normal elderly. Proc Natl Acad Sci U S A. Feb 18 2003;100(4):2019-2022.
- ^ a b Risérus U, Willett WC, Hu FB (January 2009). "Dietary fats and prevention of type 2 diabetes". Progress in Lipid Research 48 (1): 44–51. doi:10.1016/j.plipres.2008.10.002. PMC 2654180. PMID 19032965. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2654180.
- ^ 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): 29–36. PMID 19145963.
- ^ J. Nutr., Mar 2010; 140: 437 - 445.
- ^ Mozaffarian D, Kamineni A, Carnethon M, Djoussé L, Mukamal KJ, Siscovic, D (April 2009). "Lifestyle Risk Factors and New-Onset Diabetes Mellitus in Older Adults: The Cardiovascular Health Study". Archives of Internal Medicine 169 (8): 798–807. doi:10.1001/archinternmed.2009.21. PMC 2828342. PMID 19398692. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2828342.
- ^ Centers for Disease Control and Prevention (CDC) (November 2004). "Prevalence of overweight and obesity among adults with diagnosed diabetes—United States, 1988–1994 and 1999–2002". MMWR. Morbidity and Mortality Weekly Report 53 (45): 1066–8. PMID 15549021. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5345a2.htm.
- ^ Arlan Rosenbloom, Janet H Silverstein (2003). Type 2 Diabetes in Children and Adolescents: A Clinician's Guide to Diagnosis, Epidemiology, Pathogenesis, Prevention, and Treatment. American Diabetes Association, U.S.. pp. 1. ISBN 978-1580401555.
- ^ Salmerón, J.; Hu, F. B.; Manson, J. E.; Stampfer, M. J.; Colditz, G. A.; Rimm, E. B.; Willett, W. C. (2001). "Dietary fat intake and risk of type 2 diabetes in women". The American journal of clinical nutrition 73 (6): 1019–1026. PMID 11382654.
- ^ Vasanti S. Malik et al., 2010, "Sugar-Sweetened Beverages and Risk of Metabolic Syndrome and Type 2 Diabetes: A meta-analysis", Diabetes Care 33(11), 2477-2483. http://care.diabetesjournals.org/content/33/11/2477.full?sid=25e775f0-e2cd-4094-823e-214acf07dea8
- ^ Lang IA, Galloway TS, Scarlett A, et al. (September 2008). "Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults". JAMA 300 (11): 1303–10. doi:10.1001/jama.300.11.1303. PMID 18799442.
- ^ Jack L, Boseman L, Vinicor F (April 2004). "Aging Americans and diabetes. A public health and clinical response". Geriatrics 59 (4): 14–7. PMID 15086069.
- ^ Lovejoy JC (October 2002). "The influence of dietary fat on insulin resistance". Curr. Diab. Rep. 2 (5): 435–40. doi:10.1007/s11892-002-0098-y. PMID 12643169.
- ^ Hu FB (February 2003). "Sedentary lifestyle and risk of obesity and type 2 diabetes". Lipids 38 (2): 103–8. doi:10.1007/s11745-003-1038-4. PMID 12733740.
- ^ Iwasaki Y, Takayasu S, Nishiyama M, et al. (March 2008). "Is the metabolic syndrome an intracellular Cushing state? Effects of multiple humoral factors on the transcriptional activity of the hepatic glucocorticoid-activating enzyme (11beta-hydroxysteroid dehydrogenase type 1) gene". Molecular and Cellular Endocrinology 285 (1–2): 10–8. doi:10.1016/j.mce.2008.01.012. PMID 18313835.
- ^ Chiodini I, Torlontano M, Scillitani A, et al. (December 2005). "Association of subclinical hypercortisolism with type 2 diabetes mellitus: a case-control study in hospitalized patients". European Journal of Endocrinology 153 (6): 837–44. doi:10.1530/eje.1.02045. PMID 16322389.
- ^ Taniguchi T, Hamasaki A, Okamoto M (May 2008). "Subclinical hypercortisolism in hospitalized patients with type 2 diabetes mellitus". Endocrine Journal 55 (2): 429–32. doi:10.1507/endocrj.K07E-045. PMID 18362453. http://joi.jlc.jst.go.jp/JST.JSTAGE/endocrj/K07E-045?from=PubMed. [dead link]
- ^ 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 (1–2): 40–3. doi:10.1016/j.jsbmb.2008.12.022. PMID 19444934.
- ^ Farrell JB, Deshmukh A, Baghaie AA (2008). "Low testosterone and the association with type 2 diabetes". The Diabetes Educator 34 (5): 799–806. doi:10.1177/0145721708323100. PMID 18832284.
- ^ Corona, Erik. [geneworld.stanford.edu "Geneworld"]. World Wide Patterns of Genetic Risk for Disease. Stanford University. geneworld.stanford.edu. Retrieved 17 November 2011.
- ^ Gibbons, Ann (4). "Diabetes Genes Decline Out of Africa". Science 334 (6056): 583. doi:10.1126/science.334.6056.583. http://www.sciencemag.org/content/334/6056/583.full.
- ^ Sakagashira S, Sanke T, Hanabusa T, et al. (September 1996). "Missense mutation of amylin gene (S20G) in Japanese NIDDM patients". Diabetes 45 (9): 1279–81. doi:10.2337/diabetes.45.9.1279. PMID 8772735.
- ^ Cho YM, Kim M, Park KS, Kim SY, Lee HK (May 2003). "S20G mutation of the amylin gene is associated with a lower body mass index in Korean type 2 diabetic patients". Diabetes Res. Clin. Pract. 60 (2): 125–9. doi:10.1016/S0168-8227(03)00019-6. PMID 12706321. http://linkinghub.elsevier.com/retrieve/pii/S0168822703000196. Retrieved 19 July 2008.
- ^ Eberhart, M. S.; Ogden, C, Engelgau, M, Cadwell, B, Hedley, A. A., Saydah, S. H., (November 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): 1066–8. PMID 15549021. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5345a2.htm. Retrieved 19 July 2008.
- ^ Shoelson SE, Lee J, Goldfine AB (Jul 2006). "Inflammation and insulin resistance". J Clin Invest. 116 (7): 1793–801. doi:10.1172/JCI29069. PMC 1483173. PMID 16823477. http://www.ncbi.nlm.nih.gov/pubmed/16823477. Retrieved 15 July 2011.
- ^ Camastra S, Bonora E, Del Prato S, Rett K, Weck M, Ferrannini E (December 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. doi:10.1038/sj.ijo.0801072. PMID 10643689.
- ^ Cotran, Kumar, Collins; Robbins Pathologic Basis of Disease, Saunders Sixth Edition, 1999; 913-926.
- ^ Lyssenko V, Jonsson A, Almgren P, et al. (November 2008). "Clinical risk factors, DNA variants, and the development of type 2 diabetes". The New England Journal of Medicine 359 (21): 2220–32. doi:10.1056/NEJMoa0801869. PMID 19020324.
- ^ McCarthy, M. I. (December 2010). Feero, W. G.; Guttmacher, A. E.. eds. "Genomics, Type 2 Diabetes, and Obesity". The New England Journal of Medicine 363 (24): 2339–50. doi:10.1056/NEJMra0906948. PMID 21142536.
- ^ Rother KI (April 2007). "Diabetes treatment—bridging the divide". The New England Journal of Medicine 356 (15): 1499–501. doi:10.1056/NEJMp078030. PMID 17429082.
- ^ Walley AJ, Blakemore AI, Froguel P (October 2006). "Genetics of obesity and the prediction of risk for health". Human Molecular Genetics 15 Spec No 2: R124–30. doi:10.1093/hmg/ddl215. PMID 16987875.
- ^ "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.
- ^ Barrett TG (September 2001). "Mitochondrial diabetes, DIDMOAD and other inherited diabetes syndromes". Best Practice & Research. Clinical Endocrinology & Metabolism 15 (3): 325–43. doi:10.1053/beem.2001.0149. PMID 11554774.
- ^ "The origin of diabetes Don't blame your genes They may simply be getting bad instructions—from you". Economist. 3 September 2009. http://www.economist.com/sciencetechnology/displayStory.cfm?story_id=14350157.
- ^ Umapathy,C. (2011). The state and future of closed loop insulin pumps/artificial pancreas. http://etd.ohiolink.edu/send-pdf.cgi/Umapathy%20Chandravadhana.pdf?case1301604304
- ^ DIABETES april 2009, 58: 773-795
- ^ Ohtsubo, K., Chen, M.Z., Olefsky, J.M., and Marth, J.D. (2011) "Pathway to diet– and obesity–associated diabetes through attenuation of pancreatic beta cell glycosylation and glucose transport." Nature Medicine, in press.
- ^ "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%20diabetes_new.pdf. Retrieved 2011-02-20.
- ^ 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.
- ^ Harris R, Donahue K, Rathore SS, Frame P, Woolf SH, Lohr KN (February 2003). "Screening adults for type 2 diabetes: a review of the evidence for the U.S. Preventive Services Task Force". Ann. Intern. Med. 138 (3): 215–29. PMID 12558362. http://www.annals.org/cgi/pmidlookup?view=long&pmid=12558362. Retrieved 19 July 2008.
- ^ Rolka DB, Narayan KM, Thompson TJ, et al. (2001). "Performance of recommended screening tests for undiagnosed diabetes and dysglycemia". Diabetes Care 24 (11): 1899–903. doi:10.2337/diacare.24.11.1899. PMID 11679454.
- ^ Pradhan AD, Rifai N, Buring JE, Ridker PM (2007). "HbA1c Predicts Diabetes but not Cardiovascular Disease in Non-Diabetic Women". Am. J. Med. 120 (8): 720–7. doi:10.1016/j.amjmed.2007.03.022. PMC 2585540. PMID 17679132. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2585540.
- ^ 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): 722–6. PMC 2769984. PMID 20144319. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2769984.
- ^ a b "Screening: Type 2 Diabetes Mellitus in Adults". U.S. Preventive Services Task Force. 2008. http://www.uspreventiveservicestaskforce.org/uspstf/uspsdiab.htm.
- ^ Survey results of the Hungarian Diabetes Association
- ^ Raina Elley C, Kenealy T (December 2008). "Lifestyle interventions reduced the long-term risk of diabetes in adults with impaired glucose tolerance". Evid Based Med 13 (6): 173. doi:10.1136/ebm.13.6.173. PMID 19043031.
- ^ Orozco LJ, Buchleitner AM, Gimenez-Perez G, Roqué 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.
- ^ 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.
- ^ 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): 1–11. PMID 16194123. http://www.ahrq.gov/downloads/pub/evidence/pdf/impglucose/impglucose.pdf.
- ^ "Clinical Guideline:The management of type 2 diabetes (update)". http://www.nice.org.uk/guidance/index.jsp?action=byID&o=11983.
- ^ Boussageon, R; Bejan-Angoulvant, T, Saadatian-Elahi, M, Lafont, S, Bergeonneau, C, Kassaï, B, Erpeldinger, S, Wright, JM, Gueyffier, F, Cornu, C (2011 Jul 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.
- ^ 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): 15–22. doi:10.1007/s00592-009-0126-3. PMID 19495557.
- ^ a b Davis N, Forbes B, Wylie-Rosett J (June 2009). "Nutritional strategies in type 2 diabetes mellitus". Mt. Sinai J. Med. 76 (3): 257–68. doi:10.1002/msj.20118. PMID 19421969.
- ^ 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.
- ^ 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.
- ^ a b Mooradian AD, Bernbaum M, Albert SG (July 2006). "Narrative review: a rational approach to starting insulin therapy". Ann. Intern. Med. 145 (2): 125–34. PMID 16847295.
- ^ Yki-Järvinen H, Kauppila M, Kujansuu E, et al. (November 1992). "Comparison of insulin regimens in patients with non-insulin-dependent diabetes mellitus". N. Engl. J. Med. 327 (20): 1426–33. doi:10.1056/NEJM199211123272005. PMID 1406860.
- ^ Yki-Järvinen H, Ryysy L, Nikkilä K, Tulokas T, Vanamo R, Heikkilä M (March 1999). "Comparison of bedtime insulin regimens in patients with type 2 diabetes mellitus. A randomized, controlled trial". Ann. Intern. Med. 130 (5): 389–96. PMID 10068412. http://www.annals.org/cgi/pmidlookup?view=long&pmid=10068412. Retrieved 19 July 2008.
- ^ a b Holman RR, Thorne KI, Farmer AJ, et al. (October 2007). "Addition of biphasic, prandial, or basal insulin to oral therapy in type 2 diabetes". N. Engl. J. Med. 357 (17): 1716–30. doi:10.1056/NEJMoa075392. PMID 17890232. http://content.nejm.org/cgi/pmidlookup?view=short&pmid=17890232&promo=ONFLNS19. Retrieved 19 July 2008.
- ^ a b Raskin P, Allen E, Hollander P, et al. (February 2005). "Initiating insulin therapy in type 2 Diabetes: a comparison of biphasic and basal insulin analogs". Diabetes Care 28 (2): 260–5. doi:10.2337/diacare.28.2.260. PMID 15677776. http://care.diabetesjournals.org/cgi/pmidlookup?view=long&pmid=15677776. Retrieved 19 July 2008.
- ^ Malone JK, Kerr LF, Campaigne BN, Sachson RA, Holcombe JH (December 2004). "Combined therapy with insulin lispro Mix 75/25 plus metformin or insulin glargine plus metformin: a 16-week, randomized, open-label, crossover study in patients with type 2 diabetes beginning insulin therapy". Clin Ther 26 (12): 2034–44. doi:10.1016/j.clinthera.2004.12.015. PMID 15823767. http://linkinghub.elsevier.com/retrieve/pii/S0149-2918(04)00085-2. Retrieved 19 July 2008.
- ^ Horvath K, Jeitler K, Berghold A, et al. (2007). Horvath, Karl. ed. "Long-acting insulin analogues versus NPH insulin (human isophane insulin) for type 2 diabetes mellitus". Cochrane Database Syst Rev (2): CD005613. doi:10.1002/14651858.CD005613.pub3. PMID 17443605. CD005613.
- ^ Cummings DE, Flum DR (2008). "Gastrointestinal surgery as a treatment for diabetes". JAMA 299 (3): 341–3. doi:10.1001/jama.299.3.341. PMID 18212321. http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=18212321.
- ^ Folli F, Pontiroli AE, Schwesinger WH (2007). "Metabolic aspects of bariatric surgery". Med. Clin. North Am. 91 (3): 393–414, x. doi:10.1016/j.mcna.2007.01.005. PMID 17509385. http://linkinghub.elsevier.com/retrieve/pii/S0025-7125(07)00006-5.
- ^ Robert J. Tanenberg (April 1, 2005). "Gastric Bypass Surgery". Diabetes Health. http://www.diabeteshealth.com/read/2005/04/01/4261.html.
- ^ Harris MI, Flegal KM, Cowie CC, et al. (April 1998). "Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults. The Third National Health and Nutrition Examination Survey, 1988–1994". Diabetes Care 21 (4): 518–24. doi:10.2337/diacare.21.4.518. PMID 9571335.
- ^ Chang AM, Halter JB (January 2003). "Aging and insulin secretion". American Journal of Physiology. Endocrinology and Metabolism 284 (1): E7–12. doi:10.1152/ajpendo.00366.2002 (inactive 2009-10-31). PMID 12485807.
- ^ "Diabetes and Aging". Diabetes Dateline. National Institute of Diabetes and Digestive and Kidney Diseases. 2002. http://diabetes.niddk.nih.gov/about/dateline/spri02/8.htm. Retrieved 2007-05-14.
- ^ Green A, Christian Hirsch N, Pramming SK (2003). "The changing world demography of type 2 diabetes". Diabetes Metab. Res. Rev. 19 (1): 3–7. doi:10.1002/dmrr.340. PMID 12592640.
- ^ Zimmet P, Alberti KG, Shaw J (December 2001). "Global and societal implications of the diabetes epidemic". Nature 414 (6865): 782–7. doi:10.1038/414782a. PMID 11742409. http://www.nature.com/nature/journal/v414/n6865/abs/414782a.html. Retrieved 19 July 2008.
- ^ "Total Prevalence of Diabetes and Pre-diabetes". American Diabetes Association. http://www.diabetes.org/diabetes-statistics/prevalence.jsp. Retrieved 2008-11-29. [dead link]
- ^ Inzucchi SE, Sherwin RS (March 2005). "The prevention of type 2 diabetes mellitus". Endocrinol. Metab. Clin. North Am. 34 (1): 199–219, viii. doi:10.1016/j.ecl.2004.11.008. PMID 15752928.
- ^ Gerberding, Julie Louise (2007-05-24). Diabetes. Atlanta: Centres for Disease Control. http://www.cdc.gov/nccdphp/publications/aag/ddt.htm. Retrieved 2007-09-14. [verification needed]
- ^ Diabetes rates are increasing among youth National Institutes of Health (NIH), November 13, 2007
- ^ Steinberger J, Moran A, Hong CP, Jacobs DR, Sinaiko AR (2001). "Adiposity in childhood predicts obesity and insulin resistance in young adulthood". J Pediatr 138 (4): 469–73. doi:10.1067/mpd.2001.112658. PMID 11295707.
- ^ Abate, N., Chandalia, M. (2003) The impact of ethnicity on type 2 diabetes. Journal of Diabetes and Its Complications, 17, 39-58.
- ^ King, H., Aubert, R. E., & Herman, W. H. (1998). Global burden of diabetes, 1995–2025: prevalence, numerical estimates, and projections. Diabetes Care, 21, 1414– 1431.
- ^ Schultz, L.O., Bennett, P.H., Ravussin, E., Kidd, J.R., Kidd, K.K., Esparza, J., Valencia, M.E. Effects of traditional and Western environments on prevalence of type 2 diabetes in Pima Indians in Mexico and the U.S. Diabetes Care. 29 (8), 1866-1871.
- ^ Weyer, C., Bogardus, C., Mott, D. M., & Pratley, R. E. (1999). The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus. Journal of Clinical Investigation, 104, 787– 794.
- ^ Abate, N., Chandalia, M. (2003) The impact of ethnicity on type 2 diabetes. Journal of Diabetes and Its Complications, 17, 39-58.
- Diabetes mellitus type 2 at the Open Directory Project
- Type 2 Diabetes - General Information
- National Diabetes Information Clearinghouse
- Centers for Disease Control (Endocrine pathology)
Endocrine pathology: endocrine diseases (E00–E35, 240–259) Pancreas/
pituitary axesHypothalamusPituitaryThyroidEndemic goitre · Toxic nodular goitre · Toxic multinodular goiter
Height Multiple Diabetes (E10–E14, 250) Types of diabetes Blood tests Diabetes management Complications/prognosisDiabetic comas (Diabetic hypoglycemia, Diabetic ketoacidosis, Nonketotic hyperosmolar) · Diabetic angiopathy · Diabetic foot (ulcer, neuropathic arthropathy) · Diabetic myonecrosis · Diabetic nephropathy · Diabetic neuropathy · Diabetic retinopathy · Diabetic cardiomyopathy · Diabetic dermadrome (Diabetic dermopathy, Diabetic bulla, Diabetic cheiroarthropathy, Neuropathic ulcer) Lines of research
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