Pathophysiology of Type 2 Diabetes Mellitus

REJEKINE. 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", which means it is a problem with the cells that respond to insulin rather than a problem with insulin production.

Other important contributing factors:

increase in hepatic glucose production (eg, from glycogen -> glucose conversion), especially at inappropriate times (a common cause is insane levels of insulin, such that control levels of these functions in liver cells)
decrease in insulin-mediated glucose transport in (primarily) muscle and adipose tissues (receptor and post-receptor defects)
beta-cell dysfunction-loss of early phase insulin release in response to hyperglycemic stimuli
This is a more complex problem than type 1, but sometimes it is easier to treat, especially in the early years when insulin is often still produced internally. Type 2 may go unnoticed for years before diagnosis, since symptoms are usually mild (eg, no ketoacidosis, coma, etc.) and can be sporadic. However, severe complications can result from not properly managed type 2 diabetes, including renal failure, erectile dysfunction, blindness, slow healing wounds (including surgical incisions), and arterial disease, including coronary artery disease. Onset of type 2 has been most common in middle age and old age, although it became more commonly seen in adolescents and young adults due to the increase of child obesity and inactivity. This type of diabetes called MODY increasingly seen in adolescents, but is classified as diabetes due to specific causes and not as type 2 diabetes.

Type 2 diabetes mellitus is unknown etiology (ie, origin). Diabetes mellitus with a known etiology, such as other secondary diseases, known gene defects, trauma or surgery, or the effects of the drug, more appropriately called secondary diabetes mellitus or diabetes due to specific causes. Examples include diabetes mellitus as MODY or caused by hemochromatosis, pancreatic deficiency, or certain drugs (eg, long-term use of steroids).

According to the CDC, approximately 23,613,000 people in the United States, or 8% of the population, have diabetes. Total prevalence of diabetes increased 13.5% from 2005-2007. It is estimated that only 24% of undiagnosed diabetes now, down from 30% expected in 2005 and from 50% previously estimated at ca 1995.

Approximately 90-95% of all North American cases of type 2 diabetes, and about 20% of the population over age 65 have type 2 diabetes mellitus. The fraction of type 2 diabetics in other parts of the world varies substantially, almost certainly for environmental and lifestyle reasons, though this is not known in detail. Diabetes affects more than 150 million people worldwide and this number is expected to double by 2025 .. Approximately 55 percent of type 2 are obese-chronic obesity causes increased insulin resistance that can develop into diabetes, most likely because adipose tissue (especially in the abdomen around internal organs) is the source (currently identified) of the chemical signal several other tissues (hormones and cytokines ). Other studies have shown that type 2 diabetes causes obesity as a result of changes in cell metabolism and behavior of other officers crazy on insulin resistance. However, genetics plays a relatively minor role in the widespread occurrence of type 2 diabetes. It can be logically inferred from the large increase in the occurrence of type 2 diabetes who have correlated with significant changes in western lifestyles.

Type 2 diabetes mellitus is often associated with obesity, hypertension, high cholesterol (combined hyperlipidemia), and with the condition often called metabolic syndrome (also known as Syndrome X, Reavan syndrome, or CHAOS). Secondary causes of type 2 diabetes mellitus are: acromegaly, Cushing's syndrome, thyrotoxicosis, pheochromocytoma, chronic pancreatitis, and cancer drugs.

Drug-induced hyperglycemia:

Atypical antipsychotics - Alter the characteristics of receptor binding, leading to increased insulin resistance.
Beta-blockers - inhibits insulin secretion.
Calcium channel blockers - inhibits insulin secretion by interfering with the release of cytosolic calcium.
Corticosteroids - The cause of peripheral insulin resistance and gluconeogensis.
Fluoroquinolones - Inhibit insulin secretion by blocking ATP-sensitive potassium channels.
Naicin - They cause increased insulin resistance due to increased mobilization of free fatty acids.
Phenothiazines - inhibits insulin secretion.
Protease Inhibitor - Inhibiting the conversion of proinsulin to insulin.
Thiazide diuretic - inhibits secretion of insulin due to hypokalemia. They also lead to increased insulin resistance due to increased mobilization of free fatty acids.
Additional factors found to increase risk of type 2 diabetes include aging, high-fat diets and less active lifestyle ..