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Saturday, June 14, 2008

DM Type II: An Assasin Inside You

Saturday, June 14, 2008

Type 2 diabetes mellitus is considered differently due to insulin resistance or reduced insulin sensitivity, collective with reduced insulin secretion. The flawed receptiveness of body tissues to insulin more or less certainly involves the insulin receptor in cell membranes. In the early stage the predominant irregularity is reduced insulin sensitivity, characterized by high levels of insulin in the blood. At this stage hyperglycemia can be reversed by a range of measures and medications that advance insulin sensitivity or lessen glucose production by the liver. As the disease developsthe impairment of insulin secretion gets worse, and therapeutic substitution of insulin often becomes required.

There are plentiful theories as to the correct cause and mechanism in type 2 diabetes. Central obesity or fat concentrated around the waist in relation to abdominal organs, but not subcutaneous fat is known to predispose individuals for insulin resistance. Abdominal fat is particularly active hormonally, secreting a group of hormones called adipokines that may perhaps impair glucose tolerance. Obesity is found in roughly 55% of patients diagnosed with type 2 diabetes. Other reasons include aging or about 20% of elderly patients in North America have diabetes and family history (type 2 is much more frequent in those with close relatives who have had it). In the last decade, type 2 diabetes has progressively more begun to involve children and adolescents, likely in link with the increased incidence of childhood obesity seen in recent decades in some places.

Type 2 diabetes may go overlooked for years because evident symptoms are characteristically mild, non-existent or sporadic, and typically there are no ketoacidotic episodes. Conversely, severe long-term difficulties can result from disregarded 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 diabetic neuropathy, and liver damage from non-alcoholic steatohepatitis.

Type 2 diabetes is regularly first treated by rising physical activity, lessening carbohydrate intake, and losing weight. These can re-establish insulin sensitivity even when the weight loss is modest most more than ever when it is in abdominal fat deposits. It is occasionally possible to attain long-term, suitable glucose control with these measures alone. However, the original tendency to insulin resistance is not lost, and so attention to diet, exercise, and weight loss must keep on. The standard next step, if needed, is treatment with oral antidiabetic drugs. Insulin production is at first only fairly impaired in type 2 diabetes, so oral medication (often used in various combinations) can be used to improve insulin production, to regulate unsuitable release of glucose by the liver and attenuate insulin resistance to some extent, and to substantially attenuate insulin resistance. According to one study, overweight patients treated with metformin compared with diet alone, had virtual risk reductions of 32% for any diabetes endpoint, 42% for diabetes linked death and 36% for all cause mortality and stroke. Oral medication may sooner or later fail due to additional injury of beta cell insulin secretion. At this point, insulin therapy is required to maintain normal or near normal glucose levels.

These facts are critically digested from the internet and essential references.