Isomer-specific regulation of metabolism and PPARγ signaling by CLA in human preadipocytes
Copyright policy )Isomer-specific regulation of metabolism and PPARγ signaling by CLA in human preadipocytes
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 adipocytes 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 gamma (PPARgamma) and several of its downstream target genes when compared with vehicle controls. Transient transfections demonstrated that both CLA isomers antagonized ligand-dependent activation of PPARgamma. 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 PPARgamma expression.
- University of Wisconsin–Madison United States
- University of Wisconsin–Oshkosh United States
- University of North Carolina at Chapel Hill United States
- University of Southern Denmark Denmark
- University of Wisconsin System United States
Time Factors, Conjugated, Cytoplasmic and Nuclear, Antimetabolites, Oligonucleotides, Receptors, Cytoplasmic and Nuclear, Biochemistry, peroxisome proliferator-activated receptor gamma, Mice, Receptors, lipid metabolism, Adipocytes, Protein Isoforms, Linoleic Acids, Conjugated, triglycerides, Phospholipids, Cells, Cultured, Chromatography, Cultured, Reverse Transcriptase Polymerase Chain Reaction, Fatty Acids, Cell Differentiation, Linoleic Acids, Adipose Tissue, Gas, Drug, Signal Transduction, Chromatography, Gas, Cells, glucose metabolism, Immunoblotting, QD415-436, Deoxyglucose, Transfection, fatty acids, conjugated linoleic acid, Dose-Response Relationship, 3T3-L1 Cells, Animals, Humans, Triglycerides, Dose-Response Relationship, Drug, Water, Carbon Dioxide, Lipid Metabolism, Oxygen, Glucose, Gene Expression Regulation, RNA, Transcription Factors, Oleic Acid
Time Factors, Conjugated, Cytoplasmic and Nuclear, Antimetabolites, Oligonucleotides, Receptors, Cytoplasmic and Nuclear, Biochemistry, peroxisome proliferator-activated receptor gamma, Mice, Receptors, lipid metabolism, Adipocytes, Protein Isoforms, Linoleic Acids, Conjugated, triglycerides, Phospholipids, Cells, Cultured, Chromatography, Cultured, Reverse Transcriptase Polymerase Chain Reaction, Fatty Acids, Cell Differentiation, Linoleic Acids, Adipose Tissue, Gas, Drug, Signal Transduction, Chromatography, Gas, Cells, glucose metabolism, Immunoblotting, QD415-436, Deoxyglucose, Transfection, fatty acids, conjugated linoleic acid, Dose-Response Relationship, 3T3-L1 Cells, Animals, Humans, Triglycerides, Dose-Response Relationship, Drug, Water, Carbon Dioxide, Lipid Metabolism, Oxygen, Glucose, Gene Expression Regulation, RNA, Transcription Factors, Oleic Acid
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