title: Sparing effect of leptin on liver glycogen stores in rats during the fed-to-fasted transition.
abstract: 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.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
authors.forename: R M
authors.initials: RM
authors.lastname: O'Doherty
authors.forename: P R
authors.initials: PR
authors.lastname: Anderson
authors.forename: A Z
authors.initials: AZ
authors.lastname: Zhao
authors.forename: K E
authors.initials: KE
authors.lastname: Bornfeldt
authors.forename: C B
authors.initials: CB
authors.lastname: Newgard
mesh_terms: D015105:3',5'-Cyclic-AMP Phosphodiesterases / Q000378:metabolism; D000273:Adipose Tissue / Q000033:anatomy & histology; D000818:Animals; D001835:Body Weight; D054684:Cyclic Nucleotide Phosphodiesterases, Type 3; D004435:Eating / Q000502:physiology*; D004822:Epididymis; D005215:Fasting / Q000502:physiology*; D006003:Glycogen / Q000378:metabolism*; D006006:Glycogen Synthase / Q000378:metabolism; D020738:Leptin / Q000494:pharmacology*; D008099:Liver / Q000378:metabolism*; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism; D009929:Organ Size; D006005:Phosphorylases / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D001616:beta-Galactosidase / Q000494:pharmacology
chemical_list: D020738:Leptin; D006003:Glycogen; D006005:Phosphorylases; D006006:Glycogen Synthase; D015105:3',5'-Cyclic-AMP Phosphodiesterases; D054684:Cyclic Nucleotide Phosphodiesterases, Type 3; C517294:Pde3b protein, rat; D001616:beta-Galactosidase