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Studies of origins of abnormal sympathetic function in obese Zucker rats

Studies of origins of abnormal sympathetic function in obese Zucker rats BARRYE., JOSEPHANNC.. Studies of origins of abnormal in Zucker . Am. J. Physiol. 245 (Endocrinol. Metab. 8): E87E93, 1983.-To explain previously described abnormalities of in the genetically Zucker rat, the kinetics of norepinephrine (NE) metabolism were examined. Lower stress-induced levels of plasma NE in the rat were shown to be due to decreased release of NE because uptake of [“H]NE tracer from plasma was 45% slower in the compared with the rat. NE levels were 15, 20, 34% lower in heart, pancreas, interscapular brown adipose tissue (IBAT), NE turnover rates (determined by two independent methods) were 39-48 43-69% lower in the pancreas IBAT of compared with . In vivo synthesis of [“H]NE from [“Hldopamine by the enzyme dopamine phydroxylase was 60% lower in IBAT but was equal in hearts of compared with . These results suggest an organspecific decrease of NE synthesis in the Zucker rat, possibly due to decreased dopamine ,&hydroxylase activity in IBAT. obesity; catecholamine metabolism; dopamine norepinephrine turnover; brown adipose tissue ,&hydroxylase; THE GENETICALLY ZUCKER RAT has been used extensively as a model for human obesity because the two types of obesity share a number of similar physiological metabolic abnormalities (2, 3). Two important abnormalities http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Endocrinology and Metabolism The American Physiological Society

Studies of origins of abnormal sympathetic function in obese Zucker rats

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Publisher
The American Physiological Society
Copyright
Copyright © 1983 the American Physiological Society
ISSN
0193-1849
eISSN
1522-1555
Publisher site
See Article on Publisher Site

Abstract

BARRYE., JOSEPHANNC.. Studies of origins of abnormal in Zucker . Am. J. Physiol. 245 (Endocrinol. Metab. 8): E87E93, 1983.-To explain previously described abnormalities of in the genetically Zucker rat, the kinetics of norepinephrine (NE) metabolism were examined. Lower stress-induced levels of plasma NE in the rat were shown to be due to decreased release of NE because uptake of [“H]NE tracer from plasma was 45% slower in the compared with the rat. NE levels were 15, 20, 34% lower in heart, pancreas, interscapular brown adipose tissue (IBAT), NE turnover rates (determined by two independent methods) were 39-48 43-69% lower in the pancreas IBAT of compared with . In vivo synthesis of [“H]NE from [“Hldopamine by the enzyme dopamine phydroxylase was 60% lower in IBAT but was equal in hearts of compared with . These results suggest an organspecific decrease of NE synthesis in the Zucker rat, possibly due to decreased dopamine ,&hydroxylase activity in IBAT. obesity; catecholamine metabolism; dopamine norepinephrine turnover; brown adipose tissue ,&hydroxylase; THE GENETICALLY ZUCKER RAT has been used extensively as a model for human obesity because the two types of obesity share a number of similar physiological metabolic abnormalities (2, 3). Two important abnormalities

Journal

AJP - Endocrinology and MetabolismThe American Physiological Society

Published: Jul 1, 1983

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