| Acute elevation of plasma lipids does not affect ATP synthesis in human skeletal muscle. | |
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MedLine Citation:
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PMID: 20442322 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Prolonged elevation of plasma triglycerides and free fatty acids (FFA) reduces insulin-stimulated glucose disposal and myocellular flux through ATP synthase (fATPase). However, the early effects of lipids per se on fATPase are as yet unclear. Thus, this study examined glucose disposal and fATPase during 3 h of FFA elevation in the presence of low plasma insulinemia. Euglycemic pancreatic clamps with low-dose insulin supplementation (6 mU.m body surface area(-2).min(-1)) were performed in eight healthy men with (LIP) or without (CON) lipid infusion to measure whole body glucose disposal. (31)P/(1)H magnetic resonance spectroscopy of calf muscle was applied to quantify fATPase and concentrations of glucose 6-phosphate (G6P), inorganic phosphate (P(i)), phosphocreatine (PCr), ADP, pH, and IMCL before and during the clamps. Lipid infusion increased plasma FFA approximately twofold and decreased glucose disposal by approximately 50% (110-180 min: LIP 0.87 +/- 0.45 vs. CON 1.75 +/- 0.42 mg.kg(-1).min(-1), P = 0.002; means +/- SD). Intramyocellular G6P tended to rise only under control conditions, whereas PCr, ADP, pH, and IMCL remained unchanged from fasting in LIP and CON. Although P(i) concentrations increased by approximately 18%, fATPase remained unchanged from fasting during the clamps (LIP 10.2 +/- 2.2 vs. CON 10.5 +/- 2.6 micromol.g muscle(-1).min(-1), P = not significant). We conclude that 3 h of lipid elevation fail to affect ATP synthesis despite marked reduction of whole body glucose uptake. This suggests that lipid-induced insulin resistance results primarily from mechanisms decreasing glucose uptake rather than from direct interference of fatty acid metabolites with mitochondrial function. |
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Authors:
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A Brehm; M Krssák; A I Schmid; P Nowotny; W Waldhäusl; M Roden |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-05-04 |
Journal Detail:
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Title: American journal of physiology. Endocrinology and metabolism Volume: 299 ISSN: 1522-1555 ISO Abbreviation: Am. J. Physiol. Endocrinol. Metab. Publication Date: 2010 Jul |
Date Detail:
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Created Date: 2010-06-14 Completed Date: 2010-07-14 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100901226 Medline TA: Am J Physiol Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: E33-8 Citation Subset: IM |
Affiliation:
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First Medical Department, Hanusch Hospital, Vienna, Austria. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Diphosphate
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metabolism Adenosine Triphosphatases / metabolism Adenosine Triphosphate / biosynthesis*, metabolism Adult Cross-Over Studies Fatty Acids, Nonesterified / blood* Glucose / metabolism* Glucose Clamp Technique Glucosephosphate Dehydrogenase / metabolism Humans Insulin Resistance / physiology Magnetic Resonance Spectroscopy Male Muscle, Skeletal / enzymology, metabolism* Phosphates / metabolism Phosphocreatine / metabolism Random Allocation |
| Chemical | |
Reg. No./Substance:
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0/Fatty Acids, Nonesterified; 0/Phosphates; 50-99-7/Glucose; 56-65-5/Adenosine Triphosphate; 58-64-0/Adenosine Diphosphate; 67-07-2/Phosphocreatine; EC 1.1.1.49/Glucosephosphate Dehydrogenase; EC 3.6.1.-/Adenosine Triphosphatases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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