Early metabolic defects in persons at increased risk for non-insulin dependent diabetes mellitus

Article Abstract:

In non-insulin dependent diabetes mellitus (NIDDM), the body does not produce enough insulin (helps convert carbohydrates including sugars into energy) in response to food intake. To identify the first metabolic symptoms of NIDDM, the potency and secretion of bodily insulin were measured in 26 parents and siblings of NIDDM patients. Insulin potency was measured by seeing how able patients were to maintain a normal level of glucose in their blood. (Since insulin helps convert glucose to energy, patients secreting insulin with normal potency can control their own blood glucose levels; patients secreting defective insulin need external help). Siblings and parents of NIDDM patients had impaired glucose metabolism; their defect was largely accounted for by impaired storage of glucose as glycogen (a carbohydrate) and occurred in relatives with both normal and impaired metabolic rates. After ingestion of glucose, NIDDM patients failed to secrete insulin and their relatives who could not tolerate glucose secreted less than normal. Insulin secretion in response to glucose ingestion was normal in relatives who could tolerate glucose. It was concluded that impaired glucose metabolism is common in the parents and siblings of NIDDM patients, despite their normal results on oral glucose-tolerance tests.

Research, Diagnosis, Glucose metabolism

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Association of a polymorphism in the beta3-adrenergic-receptor gene with features of the insulin resistance syndrome in Finns

Article Abstract:

A mutation in a gene coding for a receptor involved in fat metabolism may play a role in the development of obesity and non-insulin-dependent diabetes mellitus (NIDDM). Genetic analysis was carried out in a group of 128 Finns with NIDDM, 207 non-diabetic Finns, and 17 pairs of siblings with normal glucose metabolism where one sibling carried the mutation on both chromosomes and the other did not. Glucose metabolism was evaluated, and measurements were made of body lean tissue, waist and hip circumference, and blood pressure. Non-diabetic participants carrying the mutation were more likely to be fatter around the waist, resistant to insulin, and to have higher blood pressure. Diabetes onset occurred at an earlier age in carriers. Siblings carrying the mutation on both chromosomes tended to be fatter than siblings who had one normal chromosome, and siblings carrying the mutation were more insulin resistant than siblings with normal genes.

Epinephrine, Adrenergic receptors

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Association between polymorphism of the glycogen synthase gene and non-insulin-dependent diabetes mellitus

Article Abstract:

Polymorphism of the glycogen synthase gene is associated with non-insulin-dependent diabetes mellitus (NIDDM) and insulin resistance. NIDDM is characterized by defective glycogen synthesis and insulin resistance and is thought to be a genetic disease. Impairment or inactivation of the gene for glycogen synthase, an enzyme involved in glycogen synthesis, might explain this defect. DNA probes of 107 patients with NIDDM and 164 non-diabetic individuals with no family history of NIDDM revealed two polymorphic alleles for the glycogen synthase gene, labelled A1 and A2. Thirty percent of the patients with NIDDM had either the A1A2 or A2A2 genotype compared with only 8% of patients without NIDDM. Diabetics with the A2 allele had a significantly greater incidence of high blood pressure and insulin resistance and had an extensive family history of NIDDM. The presence of the A2 allele could be considered an indicator of NIDDM.

Physiological aspects, Glycogen, Genetic polymorphisms, Glycogen synthesis

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