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Weight reduction increases adipose but decreases cardiac LPL in reduced-obese Zucker rats

Weight reduction increases adipose but decreases cardiac LPL in reduced-obese Zucker rats ; obesity; eride metabolism obese ; muscle; triglyc- GREENWOOD HAS SUGGESTED (l&16) that the primary event the development of some forms of obesity is not hyperphagia but rather abnormal partitiong of fuel toward storage adipose tissue relative to muscle, with hyperphagia a secondary result of this defect. She hypothesized that abnormalities adipose tissue (ATLPL) might play a central role this process. Evidence support of this hypothesis came from measurements of ATLPL activity lean, obese, and obese pair fed to lean controls (6). This study showed creased ATLPL obese relative to lean controls and no change or a mild crease pairfed . Pair-fed weighed significantly less than ad libitum-fed obese controls, but body composition, particular percent body fat, was not changed by caloric restriction. This study was done, however, without controllg for feedg effects at the time of death, and the mechanisms responsible for the crease enzyme activity were not addressed. obese humans who successfully achieve a significant E246 0193-1849/91 $1.50 Copyright reduction weight, failure to mata the weight loss is a frustratg and all too common problem. Reducedobesity is a condition where mechanisms present durg the origal development of obesity might be reexpressed. A number of studies have http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Endocrinology and Metabolism The American Physiological Society

Weight reduction increases adipose but decreases cardiac LPL in reduced-obese Zucker rats

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Publisher
The American Physiological Society
Copyright
Copyright © 1991 the American Physiological Society
ISSN
0193-1849
eISSN
1522-1555
Publisher site
See Article on Publisher Site

Abstract

; obesity; eride metabolism obese ; muscle; triglyc- GREENWOOD HAS SUGGESTED (l&16) that the primary event the development of some forms of obesity is not hyperphagia but rather abnormal partitiong of fuel toward storage adipose tissue relative to muscle, with hyperphagia a secondary result of this defect. She hypothesized that abnormalities adipose tissue (ATLPL) might play a central role this process. Evidence support of this hypothesis came from measurements of ATLPL activity lean, obese, and obese pair fed to lean controls (6). This study showed creased ATLPL obese relative to lean controls and no change or a mild crease pairfed . Pair-fed weighed significantly less than ad libitum-fed obese controls, but body composition, particular percent body fat, was not changed by caloric restriction. This study was done, however, without controllg for feedg effects at the time of death, and the mechanisms responsible for the crease enzyme activity were not addressed. obese humans who successfully achieve a significant E246 0193-1849/91 $1.50 Copyright reduction weight, failure to mata the weight loss is a frustratg and all too common problem. Reducedobesity is a condition where mechanisms present durg the origal development of obesity might be reexpressed. A number of studies have

Journal

AJP - Endocrinology and MetabolismThe American Physiological Society

Published: Aug 1, 1991

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