Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2011-5-16
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-2275
pubmed:author
pubmed:issnType
Print
pubmed:volume
52
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1247-55
pubmed:dateRevised
2011-11-17
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
pubmed:year
2011
pubmed:articleTitle
Adipose-specific disruption of autotaxin enhances nutritional fattening and reduces plasma lysophosphatidic acid.
pubmed:affiliation
Institut National de la Santé et de la Recherche Médicale (INSERM), U1048, Toulouse, Cedex 4, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't