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March 1966

Effect of Prolonged Fasting Glucose and Insulin Metabolism in Exogenous Obesity

Author Affiliations


From the Department of Medicine, University of Colorado Medical Center, Denver.

Arch Intern Med. 1966;117(3):343-347. doi:10.1001/archinte.1966.03870090027005

It HAS BECOME increasingly apparent that the metabolic abnormalities seen in exogenous obesity are complex.1 While it remains true that the most common cause of obesity is simply overeating, nevertheless various investigators have demonstrated a wide range of metabolic abnormalities, many of which could contribute to the maintenance of the obese state. The abnormalities described thus far include: impaired glucose tolerance, resistance to ketosis, impaired fatty acid mobilization with fasting or epinephrine administration, inhibition of glycolysis, increased urinary 17-ketosteroid and 17-ketogenic steroids, excessive insulin response following a glucose load, and impaired secretion of growth hormone with starvation.2-9 The purpose of this investigation was to study carbohydrate metabolism in the patient with exogenous obesity with particular reference to the influence of plasma free fatty acid (FFA) levels in accelerating or perpetuating obesity.

Methods  Twelve patients with exogenous obesity were admitted to the Clinical Research Ward of the University

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