American Journal of Clinical Nutrition, Vol 25, 746-755, Copyright © 1972 by The American Society for Clinical Nutrition, Inc.

Dissociation of the obesity-hyperinsulinism relationship following dietary restriction and hyperalimentation

¹ From the Medical Service, Veterans Administration Center (Wadsworth), Los Angeles, California 90073, and the Department of Medicine, UCLA School of Medicine, Los Angeles, California 90024

Glucose tolerance and insulin responses following glucose loads were measured in obese men, 1) during phases of high but equicaloric food intake, 2) during normal food intake, after a stable reduced weight had been established, and again 3) after a partial weight gain due to overeating. The subjects were divided into three groups who during the base-line period had either a normal, or an excessive, or a subnormal insulin response to a glucose load.

The anticipated improvement in glucose tolerance, following weight loss, was accompained by a lowering in post-glucose insulin responses in the two subgroups of men who originally had had normal or increased insulin responses. In contrast, the diabetic group, which was originally insulin deficient, manifested a rise in post-glucose insulin levels following weight loss.

Hyperalimentation, after a prolonged period at a stable reduced weight, evoked a marked deterioration in glucose disposal in all subjects including the group, which originally at a much greater weight, had been normal. Furthermore it was demonstrated during this phase that calorie excess may precipitate an increase in stimulated insulin production at a lower weight, when previously with severe obesity, a calorically balanced intake had been characterized by normal insulin responses.

Calorie excess at a lower weight may precipitate a deficiency in insulin production in subjects who previously, during stable obesity, had been hyperinsulinemic. Calorie excess after weight loss in originally insulin-deficient, obese diabetic subjects may result in transient hyperinsulinemia and this may subsequently revert to insulin deficiency. The observations suggested that the direction of change in the degree of obesity and, therefore, the direction of change in the size of fat cells need not correlate with the directional change in insulin responses. The level of food intake and the capability to secrete insulin during base-line obesity appeared to determine the patterns of post-glucose insulin responses independent of changes in body weight. The sequence of events suggests that food excess is the initial stimulus to hyperinsulinism in obesity and that peripheral tissue resistance is an adaptive response to the chronic overproduction of insulin. The data collected during the evolution and regression of "obesity diabetes" allowed the formulation of a comprehensive scheme showing the temporal relationships of variations in glucose disposal and changes in post-glucose insulin responses as a function of the level of food intake.

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