Role of reduced suppression of glucose production and diminished early insulin release in impaired glucose tolerance

Article Abstract:

Impaired insulin secretion following the ingestion of glucose may cause excessive levels of glucose in the blood of individuals with impaired glucose intolerance. The excess glucose would in turn cause increased insulin secretion. Thus, hyperglycemia (high blood sugar) rather than insulin resistance may cause the delay in insulin secretion in these individuals. Compared to 16 healthy individuals, 15 individuals with impaired glucose tolerance had greater concentrations of glucose in their blood after drinking a glucose solution. This was true in nonobese as well as obese individuals. The increase was due to glucose production by the liver, which in healthy individuals is normally suppressed. Glucose production by the liver was only suppressed 28% in those with glucose intolerance compared to 48% in the healthy individuals. This in turn was caused by impaired insulin secretion in the individuals with glucose intolerance, whose increase in insulin was smaller than the healthy individuals.

Glucose metabolism

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Carbohydrate metabolism in non-insulin-dependent diabetes mellitus

Article Abstract:

Patients with non-insulin dependent diabetes mellitus (NIDDM) have abnormalities in carbohydrate metabolism that contribute to the development of the disease. In healthy individuals, the amount of glucose (sugar) that enters the blood stream after eating is approximately equal to the amount that leaves it. Blood glucose levels are controlled by complex interactions between glucose, insulin and glucagon. Patients with NIDDM release higher levels of glucose into the blood stream after eating because they are suffering from an insulin deficiency. Uptake of glucose from the blood also occurs at a faster rate in NIDDM patients than in healthy individuals. NIDDM patients should modify their diet and receive treatment with insulin or hypoglycemic drugs to help correct abnormalities in carbohydrate metabolism. They should also exercise regularly and keep their weight within a healthy range.

Abnormalities, Carbohydrate metabolism

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Pancreatic beta-cell dysfunction as the primary genetic lesion in NIDDM: evidence from studies in normal glucose-tolerant individuals with a first-degree NIDDM relative

Article Abstract:

Genetic defects in insulin secretion rather than insulin resistance appear to be the critical factor that predisposes people to non-insulin-dependent diabetes mellitus (NIDDM). These defects cause impaired pancreatic beta-cell functioning which affects insulin secretion. Researcher evaluated 50participants with close NIDDM relatives and 50 without NIDDM relatives for, all with normal glucose tolerance, for insulin secretion and insulin resistance. Both groups consisted of people with European heritage and were similar in age, sex and obesity. Researchers found that 35% to 55% of subjects with a close NIDDM relative showed faulty response of insulin secretion when their blood sugar was raised. Only 5% to 15% showed insulin resistance, which contradicts the widely held belief that faulty insulin secretion follows insulin resistance.

Genetic aspects, Insulin resistance, Pancreatic beta cells

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