Insulin resistance means that body cells do not respond appropriately when insulin is present. Unlike type 1 diabetes mellitus, insulin resistance is generally "post-receptor", meaning it is a problem with the cells that respond to insulin rather than a problem with the production of insulin.
Other important contributing factors:
- increased hepatic glucose production (e.g., from glycogen -> glucose conversion), especially at inappropriate times (typical cause is deranged insulin levels, as those levels control this function in liver cells)
- decreased insulin-mediated glucose transport in (primarily) muscle and adipose tissues (receptor and post-receptor defects)
- impaired beta-cell function—loss of early phase of insulin release in response to hyperglycemic stimuli
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. Type 2 may go unnoticed for years before diagnosis, since symptoms are typically milder (eg, no ketoacidosis, coma, etc) and can be sporadic. However, 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 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.
Diabetes mellitus type 2 is of unknown etiology (i.e., origin). Diabetes mellitus with a known etiology, such as secondary to other diseases, known gene defects, trauma or surgery, or the effects of drugs, is more appropriately called secondary diabetes mellitus 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).
According to CDC, about 23.613 million people in the United States, or 8% of the population, have diabetes. The total prevalence of diabetes increased 13.5% from 2005-2007. It is thought that only 24% of diabetes is now undiagnosed, down from an estimated 30% in 2005 and from the previously estimated 50% in ca 1995.
About 90–95% of all North American cases of diabetes are type 2, and about 20% of the population over the age of 65 has diabetes mellitus type 2. The fraction of type 2 diabetics in other parts of the world varies substantially, almost certainly for environmental and lifestyle reasons, though these are not known in detail. Diabetes affects over 150 million people worldwide and this number is expected to double by 2025.. About 55 percent of type 2 are obese —chronic obesity leads to increased insulin resistance that can develop into diabetes, most likely because adipose tissue (especially that in the abdomen around internal organs) is a (recently identified) source of several chemical signals to other tissues (hormones and cytokines). 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, genetics play a relatively small role in the widespread occurrence of type 2 diabetes. This can be logically deduced from the huge increase in the occurrence of type 2 diabetes which has correlated with the significant change in western lifestyle.
Diabetes mellitus type 2 is often associated with 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). Secondary causes of Diabetes mellitus type 2 are: acromegaly, Cushing's syndrome, thyrotoxicosis, pheochromocytoma, chronic pancreatitis, cancer and drugs.
Drug induced hyperglycemia:
- Atypical Antipsychotics - Alter receptor binding characteristics, leading to increased insulin resistance.
- Beta-blockers - Inhibit insulin secretion.
- Calcium Channel Blockers - Inhibits secretion of insulin by interfering with cytosolic calcium release.
- Corticosteroids - Cause peripheral insulin resistance and gluconeogensis.
- Fluoroquinolones - Inhibits insulin secretion by blocking ATP sensitive potassium channels.
- Naicin - They cause increased insulin resistance due to increased free fatty acid mobilization.
- Phenothiazines - Inhibit insulin secretion.
- Protease Inhibitors - Inhibit the conversion of proinsulin to insulin.
- Thiazide Diuretics - Inhibit insulin secretion due to hypokalemia. They also cause increased insulin resistance due to increased free fatty acid mobilization.
Additional factors found to increase risk of type 2 diabetes include aging, high-fat diets and a less active lifestyle..
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