Isomer-Specific Regulation of Metabolism and PPARy Signaling by CLA in Human Preadipocytes

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Michael K. McIntosh, L.S. Keker Excellence Professor (Creator)
Ron F. Morrison, Associate Professor (Creator)
The University of North Carolina at Greensboro (UNCG )
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Abstract: Trans-10,cis-12 conjugated linoleic acid (CLA) has previously been shown to be the CLA isomer responsible for CLA-induced reductions in body fat in animal models, and we have shown that this isomer, but not the cis-9,trans-11 CLA isomer, specifically decreased triglyceride (TG) accumulation in primary human adiopcytes in vitro. Here we investigated the mechanism behind the isomer-specific, CLA-mediated reduction in TG accumulation in differentiating human preadipocytes. Trans-10,cis-12 CLA decreased insulin-stimulated glucose uptake and oxidation, and reduced insulin-dependent glucose transporter 4 gene expression. Furthermore, trans-10,cis-12 CLA reduced oleic acid uptake and oxidation when compared with all other treatments. In parallel to CLA’s effects on metabolism, trans-10,cis-12 CLA decreased, whereas cis-9,trans-11 CLA increased, the expression of peroxisome proliferator-activated receptor ? (PPAR?) and several of its downstream target genes when compared with vehicle controls. Transient transfections demonstrated that both CLA isomers antagonized ligand-dependent activation of PPAR?. Collectively, trans-10,cis-12, but not cis-9, trans-11, CLA decreased glucose and lipid uptake and oxidation and preadipocyte differentiation by altering preadipocyte gene transcription in a manner that appeared to be due, in part, to decreased PPAR? expression.

Additional Information

Journal of Lipid Research, 44(7), 1287-1300
Language: English
Date: 2003
conjugated lineoic acid, fatty acids, lipid metabolism, glucose metabolism, triglycerides, peroxisome proliferator-activated receptor gamma

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