rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2011-5-16
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pubmed:abstractText |
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)?2 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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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Dietary Fats,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Lysophospholipids,
http://linkedlifedata.com/resource/pubmed/chemical/Multienzyme Complexes,
http://linkedlifedata.com/resource/pubmed/chemical/PPAR gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphodiesterase I,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphoric Diester Hydrolases,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrophosphatases,
http://linkedlifedata.com/resource/pubmed/chemical/alkylglycerophosphoethanolamine...,
http://linkedlifedata.com/resource/pubmed/chemical/lysophosphatidic acid
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0022-2275
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
52
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1247-55
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:21421848-Adipocytes,
pubmed-meshheading:21421848-Adipose Tissue, Brown,
pubmed-meshheading:21421848-Adipose Tissue, White,
pubmed-meshheading:21421848-Adiposity,
pubmed-meshheading:21421848-Animals,
pubmed-meshheading:21421848-Blood Glucose,
pubmed-meshheading:21421848-Cell Size,
pubmed-meshheading:21421848-Dietary Fats,
pubmed-meshheading:21421848-Disease Models, Animal,
pubmed-meshheading:21421848-Female,
pubmed-meshheading:21421848-Founder Effect,
pubmed-meshheading:21421848-Gene Deletion,
pubmed-meshheading:21421848-Glucose Tolerance Test,
pubmed-meshheading:21421848-Insulin,
pubmed-meshheading:21421848-Lysophospholipids,
pubmed-meshheading:21421848-Male,
pubmed-meshheading:21421848-Mice,
pubmed-meshheading:21421848-Mice, Knockout,
pubmed-meshheading:21421848-Multienzyme Complexes,
pubmed-meshheading:21421848-Obesity,
pubmed-meshheading:21421848-PPAR gamma,
pubmed-meshheading:21421848-Phosphodiesterase I,
pubmed-meshheading:21421848-Phosphoric Diester Hydrolases,
pubmed-meshheading:21421848-Pyrophosphatases
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pubmed:year |
2011
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pubmed:articleTitle |
Adipose-specific disruption of autotaxin enhances nutritional fattening and reduces plasma lysophosphatidic acid.
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pubmed:affiliation |
Institut National de la Santé et de la Recherche Médicale (INSERM), U1048, Toulouse, Cedex 4, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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