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American Journal of Clinical Nutrition, Vol 51, 970-978, Copyright © 1990 by The American Society for Clinical Nutrition, Inc
ORIGINAL RESEARCH COMMUNICATIONS |
MU Yang, E Presta and P Bjorntorp
Obesity Research Center, St Luke's-Roosevelt Hospital Center, Columbia University, College of Physicians and Surgeons, New York, NY 10025.
Rats with diet-induced obesity starved for 8, 15, and 25 d lost liver and muscle glycogen, excess protein, and fat in proportion to duration of starvation. Fat-cell size decreased but fat-cell number did not. Upon refeeding, body fat was only partly restored, with further increase in adipocyte hyperplasia occurring in the starved obese rats. In contrast, fat-cell size was restored to near that of the prefasting value in the starved controls (dry-food-fed, fasted 4 d) after refeeding. With refeeding, food efficiency increased only if starvation had caused a reduction of adipocyte size below normal. Change in food efficiency was not associated with decreases in total carcass protein, specific tissue proteins, or glycogen stores but was correlated with degree of adipocyte filling. It is possible that adipose tissue status somehow modulates energy-dissipating mechanisms.
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