Document Detail

Response of leptin to short-term and prolonged overfeeding in humans.
MedLine Citation:
PMID:  8923877     Owner:  NLM     Status:  MEDLINE    
As one of the postulated roles of the ob gene product, leptin, is regulation of energy balance and preservation of normal body composition, we investigated the effect of acute and chronic calorie excess (weight gain) on serum leptin in humans. Two protocols were employed: 1) acute (12-h) massive (120 Cal/kg) voluntary overfeeding of eight healthy individuals; and 2) chronic overfeeding to attain 10% weight gain, with its subsequent maintenance for additional 2 weeks, involving six normal males. In the acute experiments (protocol 1), circulating leptin rose by 40% over baseline (P < 0.01) during the final hours of overfeeding; this increase persisted until the next morning. At the point of achievement and the 2-week maintenance of 10% weight gain (protocol 2), a more than 3-fold rise in the basal leptin concentration was observed (P < 0.01). A direct linear relationship was found between the magnitude of the leptin response to weight gain and the percent gain of body fat (r = 0.88; P < 0.01). In summary, 1) in contrast to normal food intake (8), short term massive overfeeding is associated with a moderate elevation of circulating leptin levels that persists until next feeding cycle is initiated; and 2) a 10% weight gain causes different changes in the body composition, and the resulting rise in circulating leptin parallels the increase in the percentage of body fat. In conclusion, these studies document acute elevation of leptin in response to positive energy balance and suggest that developing resistance to leptin is associated with bigger fat deposition during weight gain in humans.
J W Kolaczynski; J P Ohannesian; R V Considine; C C Marco; J F Caro
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  81     ISSN:  0021-972X     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  1996 Nov 
Date Detail:
Created Date:  1997-01-17     Completed Date:  1997-01-17     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  4162-5     Citation Subset:  AIM; IM    
Department of Medicine, Jefferson Medical College, USA.
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MeSH Terms
Adipose Tissue / anatomy & histology
Blood Glucose / metabolism
Energy Intake
Energy Metabolism
Insulin / blood
Proteins / metabolism*
Weight Gain / physiology*
Grant Support
Reg. No./Substance:
0/Blood Glucose; 0/Leptin; 0/Proteins; 11061-68-0/Insulin

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