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PubMed1977

Aging and insulin resistance in a group of nonobese male volunteers.

The relationship of age to insulin resistance was determined in 100 nonobese men whose ages ranged from 22 to 69 years. Seventy of the 100 subjects had normal glucose tolerance, and 30 had chemical diabetes. Insulin resistance was estimated by measuring the steady-state plasma glucose response to a continuous infusion of insulin, glucose, epinephrine, and propranolol. This approach permitted inhibition of endogenous insulin release, achievement of a comparable steady-state plasma level of exogenous insulin, and use of the height of the steady-state plasma glucose response as a direct estimate of insulin resistance. With this experimental method, no correlation was found between age and insulin resistance over the age span of the experimental population. Furthermore, there was no correlation between age and the height of the plasma glucose response to an oral glucose challenge in this population of nonobese, healthy ambulatory men.

Adult↗

PubMedDate not supplied

Diabetic hypertriglyceridemia.

The conference opened with the clinical presentation of a 50-year-old male with fasting hyperglycemia (296 mg per cent) and hypertriglyceridemia (2736 mg per cent). The discussion began with a summary of current concepts regarding the manner in which chylomicra (intestine) and very low density lipoproteins (intestine and liver) are formed, transported into the plasma, and removed from the circulation. This was followed by a consideration of diabetic hypertriglyceridemia in which this syndrome was subdivided into two categories. The first form is seen in patients with severe fasting hyperglycemia, and is characterized by marked insulin deficiency, decreased very low density lipoprotein production, a fall in the activity of lipoprotein lipase, and hypertriglyceridemia secondary to a defect in removal of lipoproteins from the plasma. In contrast the other form of diabetic hypertriglyceridemia is seen in patients with minimal abnormalities of carbohydrate tolerance, and in this instance insulin resistance, not insulin lack, seems to play the pivotal role. In these patients, the rise in plasma triglyceride levels seems to be secondary to increased production of very low density lipoproteins, presumably as a result of the hyperinsulinemia associated with the insulin resistance. The conference ended with an attempt to relate the patient presented to the models of diabetic hypertriglyceridemia that had been defined.

Animals↗