| Recovered insulin response by 2 weeks of leptin administration in high-fat fed rats is associated with restored AS160 activation and decreased reactive lipid accumulation. | |
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MedLine Citation:
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PMID: 21525176 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Leptin is an adipokine that increases fatty acid (FA) oxidation, decreases intramuscular lipid stores, and improves insulin response in skeletal muscle. In an attempt to elucidate the underlying mechanisms by which these metabolic changes occur, we administered leptin (Lep) or saline (Sal) by miniosmotic pumps to rats during the final 2 wk of a 6-wk low-fat (LF) or high-fat (HF) diet. Insulin-stimulated glucose transport was impaired by the HF diet (HF-Sal) but was restored with leptin administration (HF-Lep). This improvement was associated with restored phosphorylation of Akt and AS160 and decreased in reactive lipid species (ceramide, diacylglycerol), known inhibitors of the insulin-signaling cascade. Total muscle citrate synthase (CS) activity was increased by both leptin and HF diet, but was not additive. Leptin increased subsarcolemmal (SS) and intramyofibrillar (IMF) mitochondria CS activity. Total muscle, sarcolemmal, and mitochondrial (SS and IMF) FA transporter (FAT/CD36) protein content was significantly increased with the HF diet, but not altered by leptin. Therefore, the decrease in reactive lipid stores and subsequent improvement in insulin response, secondary to leptin administration in rats fed a HF diet was not due to a decrease in FA transport protein content or altered cellular distribution. |
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Authors:
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Leslie E Stefanyk; Roberto A Gulli; Ian R Ritchie; Adrian Chabowski; Laelie A Snook; Arend Bonen; David J Dyck |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2011-04-27 |
Journal Detail:
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Title: American journal of physiology. Regulatory, integrative and comparative physiology Volume: 301 ISSN: 1522-1490 ISO Abbreviation: Am. J. Physiol. Regul. Integr. Comp. Physiol. Publication Date: 2011 Jul |
Date Detail:
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Created Date: 2011-07-04 Completed Date: 2011-09-08 Revised Date: 2011-11-04 |
Medline Journal Info:
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Nlm Unique ID: 100901230 Medline TA: Am J Physiol Regul Integr Comp Physiol Country: United States |
Other Details:
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Languages: eng Pagination: R159-71 Citation Subset: IM |
Affiliation:
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Dept. of Human Health and Nutritional Sciences, University of Guelph, Ontario, Canada, N1G 2W1. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Body Composition / drug effects, physiology Citrate (si)-Synthase / metabolism Dietary Fats / adverse effects, pharmacology* Disease Models, Animal Dose-Response Relationship, Drug Female GTPase-Activating Proteins / metabolism* Glucose Transporter Type 4 / metabolism Insulin / metabolism* Leptin / pharmacology* Lipid Metabolism / drug effects*, physiology Mitochondria, Muscle / drug effects, physiology Muscle, Skeletal / metabolism, pathology Obesity / etiology, metabolism*, pathology Protein Kinases / metabolism Proto-Oncogene Proteins c-akt / metabolism Rats Rats, Sprague-Dawley Time Factors |
| Grant Support | |
ID/Acronym/Agency:
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//Canadian Institutes of Health Research |
| Chemical | |
Reg. No./Substance:
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0/Dietary Fats; 0/GTPase-Activating Proteins; 0/Glucose Transporter Type 4; 0/LOC686547 protein, rat; 0/Leptin; 11061-68-0/Insulin; EC 2.3.3.1/Citrate (si)-Synthase; EC 2.7.-/Protein Kinases; EC 2.7.1.-/AMP-activated protein kinase kinase; EC 2.7.11.1/Proto-Oncogene Proteins c-akt |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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