| Rosiglitazone controls fatty acid cycling in human adipose tissue by means of glyceroneogenesis and glycerol phosphorylation. | |
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MedLine Citation:
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PMID: 16524879 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Control of fatty acid homeostasis is crucial to prevent insulin resistance. During fasting, the plasma fatty acid level depends on triglyceride lipolysis and fatty acid re-esterification within fat cells. In rodents, Rosiglitazone controls fatty acid homeostasis by stimulating two pathways in the adipocytes, glyceroneogenesis and glycerol phosphorylation, that provide the glycerol 3-phosphate necessary for fatty acid re-esterification. Here, we analyzed the functionality of both pathways for controlling fatty acid release in subcutaneous adipose tissue samples from lean and overweight women before and after Rosiglitazone ex vivo treatment. In controls, pyruvate, used as a substrate of glyceroneogenesis, could contribute to the re-esterification of up to 65% of the fatty acids released after basal lipolysis, whereas glycerol phosphorylation accounted for only 14 +/- 9%. However, the efficiency of glyceroneogenesis diminished as body mass index (BMI) of women increased. After Rosiglitazone treatment, increase of either pyruvate- or glycerol-dependent fatty acid re-esterification was strictly correlated to that of phosphoenolpyruvate carboxykinase and glycerol kinase, the key enzymes of each pathway, but depended on BMI of the women. Whereas the Rosiglitazone responsiveness of glyceroneogenesis was rather constant according to the BMI of the women, glycerol phosphorylation was mostly enhanced in lean women (BMI < 27). Overall, these data indicate that, whereas glyceroneogenesis is more utilized than glycerol phosphorylation for fatty acid re-esterification in human subcutaneous adipose tissue in the physiological situation, both are solicited in response to Rosiglitazone but with lower efficiency when BMI is increased. |
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Authors:
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Stéphanie N Leroyer; Joan Tordjman; Geneviève Chauvet; Joëlle Quette; Charles Chapron; Claude Forest; Bénédicte Antoine |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2006-03-08 |
Journal Detail:
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Title: The Journal of biological chemistry Volume: 281 ISSN: 0021-9258 ISO Abbreviation: J. Biol. Chem. Publication Date: 2006 May |
Date Detail:
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Created Date: 2006-05-08 Completed Date: 2006-07-18 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 2985121R Medline TA: J Biol Chem Country: United States |
Other Details:
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Languages: eng Pagination: 13141-9 Citation Subset: IM |
Affiliation:
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INSERM-UMR-S 530/747, Université Paris Descartes, 45 Rue des Saints-Pères, 75006 Paris, France. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Adipose Tissue
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drug effects*,
metabolism* Adult Body Weight Fatty Acids / pharmacology* Female Glycerol / metabolism* Glycerol Kinase / metabolism Humans Hypoglycemic Agents / pharmacology Phosphorylation / drug effects Pyruvates / metabolism Thiazolidinediones / pharmacology* |
| Chemical | |
Reg. No./Substance:
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0/Fatty Acids; 0/Hypoglycemic Agents; 0/Pyruvates; 0/Thiazolidinediones; 122320-73-4/rosiglitazone; 56-81-5/Glycerol; EC 2.7.1.30/Glycerol Kinase |
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