Dietary factors also influence the risk of developing type 2 diabetes. Consumption of sugar-sweetened drinks in excess is associated with an increased risk.[32][33] The type of fats in the diet are important, with saturated fats and trans fatty acids increasing the risk, and polyunsaturated and monounsaturated fat decreasing the risk.[26] Eating a lot of white rice appears to play a role in increasing risk.[34] A lack of exercise is believed to cause 7% of cases.[35] Persistent organic pollutants may play a role.[36]

Clear evidence suggests a genetic component in type 1 diabetes mellitus. Monozygotic twins have a 60% lifetime concordance for developing type 1 diabetes mellitus, although only 30% do so within 10 years after the first twin is diagnosed. In contrast, dizygotic twins have only an 8% risk of concordance, which is similar to the risk among other siblings.


^ Jump up to: a b Petzold A, Solimena M, Knoch KP (October 2015). "Mechanisms of Beta Cell Dysfunction Associated With Viral Infection". Current Diabetes Reports (Review). 15 (10): 73. doi:10.1007/s11892-015-0654-x. PMC 4539350. PMID 26280364. So far, none of the hypotheses accounting for virus-induced beta cell autoimmunity has been supported by stringent evidence in humans, and the involvement of several mechanisms rather than just one is also plausible.
Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/l (110 to 125 mg/dl) are considered to have impaired fasting glucose.[67] people with plasma glucose at or above 7.8 mmol/l (140 mg/dl), but not over 11.1 mmol/l (200 mg/dl), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease.[68] The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/l (100 to 125 mg/dl).[69]
Oral medications are available to lower blood glucose in Type II diabetics. In 1990, 23.4 outpatient prescriptions for oral antidiabetic agents were dispensed. By 2001, the number had increased to 91.8 million prescriptions. Oral antidiabetic agents accounted for more than $5 billion dollars in worldwide retail sales per year in the early twenty-first century and were the fastest-growing segment of diabetes drugs. The drugs first prescribed for Type II diabetes are in a class of compounds called sulfonylureas and include tolbutamide, tolazamide, acetohexamide, and chlorpropamide. Newer drugs in the same class are now available and include glyburide, glimeperide, and glipizide. How these drugs work is not well understood, however, they seem to stimulate cells of the pancreas to produce more insulin. New medications that are available to treat diabetes include metformin, acarbose, and troglitizone. The choice of medication depends in part on the individual patient profile. All drugs have side effects that may make them inappropriate for particular patients. Some for example, may stimulate weight gain or cause stomach irritation, so they may not be the best treatment for someone who is already overweight or who has stomach ulcers. Others, like metformin, have been shown to have positive effects such as reduced cardiovascular mortality, but but increased risk in other situations. While these medications are an important aspect of treatment for Type II diabetes, they are not a substitute for a well planned diet and moderate exercise. Oral medications have not been shown effective for Type I diabetes, in which the patient produces little or no insulin.
^ Jump up to: a b Funnell, Martha M.; Anderson, Robert M. (2008). "Influencing self-management: from compliance to collaboration". In Feinglos, Mark N.; Bethel, M. Angelyn. Type 2 diabetes mellitus: an evidence-based approach to practical management. Contemporary endocrinology. Totowa, NJ: Humana Press. p. 462. ISBN 978-1-58829-794-5. OCLC 261324723.
The classic oral glucose tolerance test measures blood glucose levels five times over a period of three hours. Some physicians simply get a baseline blood sample followed by a sample two hours after drinking the glucose solution. In a person without diabetes, the glucose levels rise and then fall quickly. In someone with diabetes, glucose levels rise higher than normal and fail to come back down as fast.

By simultaneously considering insulin secretion and insulin action in any given individual, it becomes possible to account for the natural history of diabetes in that person (e.g., remission in a patient with T1 diabetes or ketoacidosis in a person with T2DM). Thus, diabetes mellitus may be the result of absolute insulin deficiency, or of absolute insulin resistance, or a combination of milder defects in both insulin secretion and insulin action.1 Collectively, the syndromes of diabetes mellitus are the most common endocrine/metabolic disorders of childhood and adolescence. The application of molecular biologic tools continues to provide remarkable insights into the etiology, pathophysiology, and genetics of the various forms of diabetes mellitus that result from deficient secretion of insulin or its action at the cellular level.


In autoimmune diseases, such as type 1 diabetes, the immune system mistakenly manufactures antibodies and inflammatory cells that are directed against and cause damage to patients' own body tissues. In persons with type 1 diabetes, the beta cells of the pancreas, which are responsible for insulin production, are attacked by the misdirected immune system. It is believed that the tendency to develop abnormal antibodies in type 1 diabetes is, in part, genetically inherited, though the details are not fully understood.
Type 1 diabetes mellitus can occur at any age, but incidence rates generally increase with age until midpuberty and then decline. [32] Onset in the first year of life, although unusual, can occur, so type 1 diabetes mellitus must be considered in any infant or toddler, because these children have the greatest risk for mortality if diagnosis is delayed. (Because diabetes is easily missed in an infant or preschool-aged child, if in doubt, check the urine for glucose.) Symptoms in infants and toddlers may include the following:

Type 2 diabetes is a progressive, chronic disease related to your body's challenges with regulating blood sugar. It is often associated with generalized inflammation. Your pancreas produces the hormone insulin to convert sugar (glucose) to energy that you either use immediately or store. With type 2 diabetes, you are unable to use that insulin efficiently. Although your body produces the hormone, either there isn't enough of it to keep up with the amount of glucose in your system, or the insulin being produced isn't being used as well as it should be, both of which result in high blood sugar levels.


It is clearly established that diabetes mellitus is not a single disease but a genetically heterogeneous group of disorders that share glucose intolerance in common (4–7). The concept of genetic heterogeneity (i.e. that different genetic and/or environmental etiologic factors can result in similar phenotypes) has significantly altered the genetic analysis of this common disorder. Diabetes and glucose intolerance are not diagnostic terms, but, like anemia, simply describe symptoms and/or laboratory abnormalities that can have a number of distinct etiologies.
They may need to take medications in order to keep glucose levels within a healthy range. Medications for type 2 diabetes are usually taken by mouth in the form of tablets and should always be taken around meal times and as prescribed by the doctor. However, if blood glucose is not controlled by oral medications, a doctor may recommend insulin injections.

You can develop type 2 diabetes at any age, even during childhood. However, type 2 diabetes occurs most often in middle-aged and older people. You are more likely to develop type 2 diabetes if you are age 45 or older, have a family history of diabetes, or are overweight or obese. Diabetes is more common in people who are African American, Hispanic/Latino, American Indian, Asian American, or Pacific Islander.
When your blood sugar is out of whack, you just don’t feel well, says Cypress, and might become more short-tempered. In fact, high blood sugar can mimic depression-like symptoms. “You feel very tired, you don’t feel like doing anything, you don’t want to go out, you just want to sleep,” Cypress says. She’ll see patients who think they need to be treated for depression, but then experience mood improvement after their blood sugar normalizes.
Diabetic peripheral neuropathy is a condition where nerve endings, particularly in the legs and feet, become less sensitive. Diabetic foot ulcers are a particular problem since the patient does not feel the pain of a blister, callous, or other minor injury. Poor blood circulation in the legs and feet contribute to delayed wound healing. The inability to sense pain along with the complications of delayed wound healing can result in minor injuries, blisters, or callouses becoming infected and difficult to treat. In cases of severe infection, the infected tissue begins to break down and rot away. The most serious consequence of this condition is the need for amputation of toes, feet, or legs due to severe infection.

There are many types of sugar. Some sugars are simple, and others are complex. Table sugar (sucrose) is made of two simpler sugars called glucose and fructose. Milk sugar (lactose) is made of glucose and a simple sugar called galactose. The carbohydrates in starches, such as bread, pasta, rice, and similar foods, are long chains of different simple sugar molecules. Sucrose, lactose, carbohydrates, and other complex sugars must be broken down into simple sugars by enzymes in the digestive tract before the body can absorb them.
In 2013, of the estimated 382 million people with diabetes globally, more than 80 per cent lived in LMIC. It was estimated that India had 65.1 million adults with diabetes in 2013, and had the 2nd position among the top 10 countries with the largest number of diabetes. This number is predicted to increase to 109 million by 2035 unless steps are taken to prevent new cases of diabetes1. Primary prevention of diabetes is feasible and strategies such as lifestyle modification are shown to be effective in populations of varied ethnicity2,3. However, for implementation of the strategies at the population level, national programmes which are culturally and socially acceptable and practical have to be formulated which are currently lacking in most of the developed and developing countries. Early diagnosis and institution of appropriate therapeutic measures yield the desired glycaemic outcomes and prevent the vascular complications4.
nephrogenic diabetes insipidus a rare form caused by failure of the renal tubules to reabsorb water; there is excessive production of antidiuretic hormone but the tubules fail to respond to it. Characteristics include polyuria, extreme thirst, growth retardation, and developmental delay. The condition does not respond to exogenous vasopressin. It may be inherited as an X-linked trait or be acquired as a result of drug therapy or systemic disease.
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus (IDDM). Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature.[citation needed]
Type 2 diabetes is believed to have a strong genetic link, meaning that it tends to run in families. Several genes are being studied that may be related to the cause of type 2 diabetes. If you have any of the following type 2 diabetes risk factors, it’s important to ask your doctor about a diabetes test. With a proper diabetes diet and healthy lifestyle habits, along with diabetes medication, if necessary, you can manage type 2 diabetes just like you manage other areas of your life. Be sure to continue seeking the latest information on type 2 diabetes as you become your own health advocate.
Monogenic diabetes is caused by mutations, or changes, in a single gene. These changes are usually passed through families, but sometimes the gene mutation happens on its own. Most of these gene mutations cause diabetes by making the pancreas less able to make insulin. The most common types of monogenic diabetes are neonatal diabetes and maturity-onset diabetes of the young (MODY). Neonatal diabetes occurs in the first 6 months of life. Doctors usually diagnose MODY during adolescence or early adulthood, but sometimes the disease is not diagnosed until later in life.
Endocrinology is the specialty of medicine that deals with hormone disturbances, and both endocrinologists and pediatric endocrinologists manage patients with diabetes. People with diabetes may also be treated by family medicine or internal medicine specialists. When complications arise, people with diabetes may be treated by other specialists, including neurologists, gastroenterologists, ophthalmologists, surgeons, cardiologists, or others.
Intensive blood sugar lowering (HbA1c<6%) as opposed to standard blood sugar lowering (HbA1c of 7–7.9%) does not appear to change mortality.[74][75] The goal of treatment is typically an HbA1c of 7 to 8% or a fasting glucose of less than 7.2 mmol/L (130 mg/dl); however these goals may be changed after professional clinical consultation, taking into account particular risks of hypoglycemia and life expectancy.[59][76][77] Despite guidelines recommending that intensive blood sugar control be based on balancing immediate harms with long-term benefits, many people – for example people with a life expectancy of less than nine years who will not benefit, are over-treated.[78]

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