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Effect of Prolonged Fasting Glucose and Insulin Metabolism in Exogenous Obesity
KARL E. SUSSMAN, MD
Arch Intern Med. 1966;117(3):343-347.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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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
. . . [Full Text PDF of this Article]
Author Affiliations
DENVER
From the Department of Medicine, University of Colorado Medical Center, Denver.
Footnotes
Received for publication July 30, 1965; accepted Oct 18.
Read before the 46th Annual Session of the American College of Physicians, Chicago, March 22, 1965.
Reprint requests to 4200 E Ninth Ave, Denver, Colo 80220.
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