Conjugated Linoleic Acid Induces Uncoupling Protein 1 in White Adipose Tissue of <Emphasis Type="Italic">ob/ob</Emphasis> Mice |
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Authors: | Angela A Wendel Aparna Purushotham Li-Fen Liu Martha A Belury |
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Affiliation: | (1) Department of Human Nutrition, The Ohio State University, 1787 Neil Avenue, Columbus, OH 43210, USA;(2) Present address: Department of Nutrition, University of North Carolina, Chapel Hill, NC 27599, USA;(3) Present address: Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA;(4) Present address: Division of Endocrinology, Stanford University, Palo Alto, CA, USA; |
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Abstract: | Conjugated linoleic acid (CLA) reduces body weight and adipose mass in a variety of species. The mechanisms by which CLA depletes
adipose mass are unclear, but two independent microarray analyses indicate that in white adipose tissue (WAT), uncoupling
protein 1 (UCP1) was among genes most changed by CLA. The objective of this study was to determine whether CLA induces ectopic
expression of UCP1 in WAT, which may contribute to increased energy expenditure and weight loss. Six-week old, male ob/ob mice were fed either a control diet (CON) or a diet supplemented with 1.5% mixed isomer CLA (CLA) for 4 weeks. A third group
of mice (LEPTIN) was fed the control diet and received daily injections of recombinant leptin as a positive control for adipose
depletion in ob/ob mice. CLA did not alter several mRNA markers of lipid oxidation in epididymal white adipose tissue (eWAT) , but significantly
increased carnitine palmitoyltransferase-1b (CPT1b) and PPAR gamma coactivator-1α (PGC1α) expression. Notably, CLA increased
both mRNA and protein expression of uncoupling protein-1 (UCP1). β3-adrenoceptor mRNA and phosphorylated-p38 mitogen activated
protein kinase (MAPK) protein levels were not affected by CLA, but were upregulated by LEPTIN. These data suggest the increased
CPT1b, PGC1α, and UCP1, in WAT of CLA-fed mice may contribute to the depletion of adipose, and CLA does not appear to increase
UCP1 through β3-adrenergic signaling. Future studies will focus on understanding how CLA increases mitochondrial oxidation
and energy dissipation in white adipose tissue. |
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