| Adipose-specific disruption of autotaxin enhances nutritional fattening and reduces plasma lysophosphatidic acid. | |
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MedLine Citation:
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PMID: 21421848 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Autotaxin (ATX) is a secreted lysophospholipase D that generates the lipid mediator lysophosphatidic acid (LPA). ATX is secreted by adipose tissue and its expression is enhanced in obese/insulin-resistant individuals. Here, we analyzed the specific contribution of adipose-ATX to fat expansion associated with nutritional obesity and its consequences on plasma LPA levels. We established ATX(F/F)/aP2-Cre (FATX-KO) transgenic mice carrying a null ATX allele specifically in adipose tissue. FATX-KO mice and their control littermates were fed either a normal or a high-fat diet (HFD) (45% fat) for 13 weeks. FATX-KO mice showed a strong decrease (up to 90%) in ATX expression in white and brown adipose tissue, but not in other ATX-expressing organs. This was associated with a 38% reduction in plasma LPA levels. When fed an HFD, FATX-KO mice showed a higher fat mass and a higher adipocyte size than control mice although food intake was unchanged. This was associated with increased expression of peroxisome proliferator-activated receptor (PPAR)γ2 and of PPAR-sensitive genes (aP2, adiponectin, leptin, glut-1) in subcutaneous white adipose tissue, as well as in an increased tolerance to glucose. These results show that adipose-ATX is a negative regulator of fat mass expansion in response to an HFD and contributes to plasma LPA levels. |
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Authors:
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Rodolphe Dusaulcy; Chloé Rancoule; Sandra Grès; Estelle Wanecq; André Colom; Charlotte Guigné; Laurens A van Meeteren; Wouter H Moolenaar; Philippe Valet; Jean Sébastien Saulnier-Blache |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2011-03-18 |
Journal Detail:
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Title: Journal of lipid research Volume: 52 ISSN: 0022-2275 ISO Abbreviation: J. Lipid Res. Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-05-16 Completed Date: 2011-09-19 Revised Date: 2011-11-07 |
Medline Journal Info:
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Nlm Unique ID: 0376606 Medline TA: J Lipid Res Country: United States |
Other Details:
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Languages: eng Pagination: 1247-55 Citation Subset: IM |
Affiliation:
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Institut National de la Santé et de la Recherche Médicale (INSERM), U1048, Toulouse, Cedex 4, France. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adipocytes
/
cytology,
metabolism Adipose Tissue, Brown / metabolism*, physiopathology Adipose Tissue, White / metabolism*, physiopathology Adiposity* Animals Blood Glucose / analysis Cell Size Dietary Fats / adverse effects, metabolism Disease Models, Animal* Female Founder Effect Gene Deletion Glucose Tolerance Test Insulin / blood Lysophospholipids* / blood Male Mice Mice, Knockout Multienzyme Complexes* / deficiency, genetics Obesity / genetics, metabolism*, physiopathology PPAR gamma / antagonists & inhibitors, genetics, metabolism* Phosphodiesterase I* / deficiency, genetics Pyrophosphatases* / deficiency, genetics |
| Chemical | |
Reg. No./Substance:
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0/Blood Glucose; 0/Dietary Fats; 0/Lysophospholipids; 0/Multienzyme Complexes; 0/PPAR gamma; 11061-68-0/Insulin; 22002-87-5/lysophosphatidic acid; EC 3.1.4.1/Phosphodiesterase I; EC 3.1.4.39/alkylglycerophosphoethanolamine phosphodiesterase; EC 3.6.1.-/Pyrophosphatases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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