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Papers In Press, published online ahead of print May 1, 2003
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Department of Nutrition, University of North Carolina at Greensboro, Greensboro, NC 27402-6170
Corresponding Author: mkmcinto{at}uncg.edu
Trans-10, cis-12 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 adipocytes. Trans-10, cis-12 CLA decreased insulin-stimulated glucose uptake and oxidation, and reduced insulin-dependent glucose transporter 4 (GLUT4) gene expression. Furthermore, trans-10, cis-12 CLA reduced oleic acid uptake and oxidation when compared to 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 gamma (PPAR)and several of its downstream target genes, when compared to 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.
Revised on April 25, 2003
Accepted on April 28, 2003
Trans-10, cis-12 conjugated linoleic acid decreases glucose and fatty acid uptake and oxidation and inhibits PPARgamma-dependent gene expression in human preadipocytes
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