| Endocrine control of oleic acid and glucose metabolism in rainbow trout (Oncorhynchus mykiss) muscle cells in culture. | |
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MedLine Citation:
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PMID: 20484701 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The effects of insulin and IGF-I on fatty acid (FA) and glucose metabolism were examined using oleic acid or glucose as tracers in differentiated rainbow trout (Oncorhynchus mykiss) myotubes. Insulin and IGF-I significantly reduced the production of CO(2) from oleic acid with respect to the control values. IGF-I also significantly reduced the production of acid-soluble products (ASP) and the concentration of FA in the medium, while cellular triacylglycerols (TAG) tended to increase. Only insulin produced a significant accumulation of glycogen inside the cells in glucose distribution experiments. Incubation with catecholamines did not affect oleic acid metabolism. Cells treated with rapamycin [a target of rapamycin (TOR) inhibitor] significantly increased the oxidation of oleic acid to CO(2) and ASP, while the accumulation of TAG diminished. Rosiglitazone (a peroxisome proliferator-activated receptor gamma agonist) and etomoxir (a CPT-1 inhibitor) produced a severe and significant reduction in the production of CO(2) and ASP. Rosiglitazone and etomoxir also produced a significant accumulation of FA outside and inside the cells, respectively. No significant effects of these drugs on glucose distribution were observed. These data indicate that insulin and IGF-I act as anabolic hormones in trout myotubes in both oleic acid and glucose metabolism, although glucose oxidation appears to be less sensitive than FA oxidation to insulin and IGF-I. The use of rapamycin, etomoxir, and rosiglitazone may help us to understand the mechanisms of regulation of lipid metabolism in fish. |
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Authors:
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Joan Sánchez-Gurmaches; Lourdes Cruz-Garcia; Joaquím Gutiérrez; Isabel Navarro |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-05-19 |
Journal Detail:
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Title: American journal of physiology. Regulatory, integrative and comparative physiology Volume: 299 ISSN: 1522-1490 ISO Abbreviation: Am. J. Physiol. Regul. Integr. Comp. Physiol. Publication Date: 2010 Aug |
Date Detail:
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Created Date: 2010-08-03 Completed Date: 2010-09-08 Revised Date: - |
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: R562-72 Citation Subset: IM |
Affiliation:
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Dept. de Fisiologia, Facultat de Biologia, Universitat de Barcelona, Catalunya, Spain. juansangu@gmail.com |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Carbon Dioxide / metabolism Carnitine O-Palmitoyltransferase / antagonists & inhibitors, metabolism Catecholamines / metabolism Cells, Cultured Energy Metabolism* / drug effects Epoxy Compounds / pharmacology Glucose / metabolism* Glycogen / metabolism Hypoglycemic Agents / pharmacology Insulin / metabolism* Insulin-Like Growth Factor I / metabolism* Intracellular Signaling Peptides and Proteins / antagonists & inhibitors, metabolism Muscle Fibers, Skeletal / drug effects, metabolism* Oleic Acid / metabolism* Oncorhynchus mykiss / metabolism* Oxidation-Reduction PPAR gamma / agonists, metabolism Protein Kinase Inhibitors / pharmacology Protein-Serine-Threonine Kinases / antagonists & inhibitors, metabolism Sirolimus / pharmacology Thiazolidinediones / pharmacology Triglycerides / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Catecholamines; 0/Epoxy Compounds; 0/Hypoglycemic Agents; 0/Intracellular Signaling Peptides and Proteins; 0/PPAR gamma; 0/Protein Kinase Inhibitors; 0/Thiazolidinediones; 0/Triglycerides; 11061-68-0/Insulin; 112-80-1/Oleic Acid; 122320-73-4/rosiglitazone; 124-38-9/Carbon Dioxide; 50-99-7/Glucose; 53123-88-9/Sirolimus; 67763-96-6/Insulin-Like Growth Factor I; 82258-36-4/etomoxir; 9005-79-2/Glycogen; EC 2.3.1.21/Carnitine O-Palmitoyltransferase; EC 2.7.1.-/mTOR protein; EC 2.7.11.1/Protein-Serine-Threonine Kinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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