Document Detail


Sparing effect of leptin on liver glycogen stores in rats during the fed-to-fasted transition.
MedLine Citation:
PMID:  10484368     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The effect of moderate hyperleptinemia ( approximately 20 ng/ml) on liver and skeletal muscle glycogen metabolism was examined in Wistar rats. Animals were studied approximately 90 h after receiving recombinant adenoviruses encoding rat leptin (AdCMV-leptin) or beta-galactosidase (AdCMV-betaGal). Liver and skeletal muscle glycogen levels in the fed and fasted (18 h) states were similar in AdCMV-leptin- and AdCMV-betaGal-treated rats. However, after delivery of a glucose bolus, liver glycogen levels were significantly greater in AdCMV-leptin compared with AdCMV-betaGal rats (P < 0.05). To investigate the mechanism(s) of these differences, glycogen levels were measured immediately after the cessation of a 3- or 6-h glucose infusion or 3, 6, and 9 h after the cessation of a 6-h glucose infusion. Similar increases in liver and skeletal muscle glycogen occurred in hyperleptinemic and control rats in response to glucose infusions. However, 3 and 6 h after the cessation of a glucose infusion, liver glycogen levels were approximately twofold greater (P < 0.05) in AdCMV-leptin-treated compared with AdCMV-betaGal-treated animals. Skeletal muscle glycogen levels were similar in AdCMV-leptin-treated and AdCMV-betaGal-treated animals at the same time points. Glycogen phosphorylase, phosphodiesterase 3B, and glycogen synthase activities were unaltered by hyperleptinemia. We conclude that moderate increases in plasma leptin levels decrease liver glycogen degradation during the fed-to-fasted transition.
Authors:
R M O'Doherty; P R Anderson; A Z Zhao; K E Bornfeldt; C B Newgard
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  277     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1999 Sep 
Date Detail:
Created Date:  1999-10-28     Completed Date:  1999-10-28     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  E544-50     Citation Subset:  IM    
Affiliation:
Gifford Laboratories for Diabetes Research and Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, Texas 75235, USA. Odohertyr@msx.dept-med.Pitt.edu
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MeSH Terms
Descriptor/Qualifier:
3',5'-Cyclic-AMP Phosphodiesterases / metabolism
Adipose Tissue / anatomy & histology
Animals
Body Weight
Cyclic Nucleotide Phosphodiesterases, Type 3
Eating / physiology*
Epididymis
Fasting / physiology*
Glycogen / metabolism*
Glycogen Synthase / metabolism
Leptin / pharmacology*
Liver / metabolism*
Male
Muscle, Skeletal / drug effects,  metabolism
Organ Size
Phosphorylases / metabolism
Rats
Rats, Wistar
beta-Galactosidase / pharmacology
Grant Support
ID/Acronym/Agency:
P30-DK-17047/DK/NIDDK NIH HHS; P50-H2598801//PHS HHS
Chemical
Reg. No./Substance:
0/Leptin; 9005-79-2/Glycogen; EC 2.4.1.-/Phosphorylases; EC 2.4.1.11/Glycogen Synthase; EC 3.1.4.17/3',5'-Cyclic-AMP Phosphodiesterases; EC 3.1.4.17/Cyclic Nucleotide Phosphodiesterases, Type 3; EC 3.1.4.17/Pde3b protein, rat; EC 3.2.1.23/beta-Galactosidase

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