Sunday, September 9, 2007

Diabetes Tyypes - Type 2 diabetes mellitus

Type 2 diabetes mellitus

Type 2 diabetes mellitus—previously known as adult-onset diabetes, maturity-onset diabetes, or non-insulin-dependent diabetes mellitus (NIDDM)—is due to a combination of defective insulin secretion and insulin resistance or reduced insulin sensitivity (defective responsiveness of tissues to insulin), which 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 reversed by a variety of measures and medications that improve insulin sensitivity or reduce glucose production by the liver, but as the disease progresses the impairment of insulin secretion worsens, and therapeutic replacement of insulin often becomes necessary. There are numerous theories as to the exact cause and mechanism for this resistance, but central obesity (fat concentrated around the waist in relation to abdominal organs, and not subcutaneous fat, it seems) is known to predispose individuals for insulin resistance, possibly due to its secretion of adipokines (a group of hormones) that impair glucose tolerance. Abdominal fat is especially active hormonally. Obesity is found in approximately 55% of patients diagnosed with type 2 diabetes.[13] Other factors include aging (about 20% of elderly patients are diabetic in North America) and family history (type 2 is much more common in those with close relatives who have had it), although in the last decade it has increasingly begun to affect children and adolescents[citation needed], likely in connection with the greatly increased childhood obesity[citation needed] seen in recent decades in some places.

Type 2 diabetes may go unnoticed for years in a patient before diagnosis, as visible symptoms are typically mild or non-existent, usually without ketoacidotic episodes, and can be sporadic as well. However, severe long-term complications can result from unnoticed type 2 diabetes, including renal failure due to diabetic nephropathy, vascular disease (including coronary artery disease), vision damage due to diabetic retinopathy, loss of sensation or pain due to diabetes neuropathy, liver damage from non-alcoholic steatohepatitis, etc.

Type 2 diabetes is usually first treated by attempts to change physical activity (generally an increase is desired), the diet (generally to decrease carbohydrate intake), and weight loss. These can restore insulin sensitivity, even when the weight loss is modest, for example, around 5 kg (10 to 15 lb), most especially when it is in abdominal fat deposits. Some type 2 diabetics can achieve satisfactory glucose control, sometimes for years, as a result. However, the underlying tendency to insulin resistance is not lost, and so attention to diet, exercise, and weight loss must continue. The usual next step, if necessary, is treatment with oral antidiabetic drugs. As insulin production is initially only moderately impaired in type 2 diabetics, oral medication (often used in various combinations) can still be used to improve insulin production (e.g., sulfonylureas), to regulate inappropriate release of glucose by the liver (and attenuate insulin resistance to some extent (e.g., metformin), and to substantially attenuate insulin resistance (e.g., thiazolidinediones). According to one study, overweight patients treated with metformin compared with diet alone, had relative risk reductions of 32% for any diabetes endpoint, 42% for diabetes related death and 36% for all cause mortality and stroke.[14] When oral medications fail (cessation of beta cell insulin secretion is not uncommon amongst Type 2s), insulin therapy will be necessary to maintain normal or near normal glucose levels. A disciplined regimen of blood glucose checks is recommended, most particularly and necessarily when taking medications