mediates the lipolytic effects of dietary fish oil to reduce body fat deposition1Y. H. Yu*, P. H. Wang*, W. T. K. Cheng
, H. J. Mersmann*,2, S. C. Wu*,3 and S. T. Ding*,3 [size=-1]* Department of Animal Science and Technology/Institute of Biotechnology, National Taiwan University, Taipei 106, Taiwan; and
Department of Animal Science and Biotechnology, Tunghai University, Taichung 407, Taiwan [size=-1]3 Corresponding authors: sding@ntu.edu.tw and scw01@ntu.edu.tw Peroxisome proliferator-activated receptor
promotes fatty acid catabolism and energy expenditure in skeletal muscle and adipose tissues. A ligand for PPAR
is required to activate PPAR
function. Polyunsaturated fatty acids are potential ligands for PPAR
activation. The current experiment was designed to determine the potential for PUFA, particularly from dietary fish oil, to activate porcine PPAR
in vivo. Transgenic mice were generated to overexpress porcine PPAR
in the adipose tissue. Mice were fed a high-saturated fat (13% beef tallow), or high-unsaturated fat (13% fish oil) diet, or a diet containing 4 mg/kg of a PPAR
ligand (L165041) for 4 mo. Compared with beef tallow feeding, fish oil feeding reduced fat mass and decreased (P < 0.05) plasma triacylglycerol and FFA concentrations in the transgenic mice. Adipose tissue expression of genes involved in adipogenesis (i.e., lipoprotein lipase and adipocyte fatty acid-binding protein) was decreased in transgenic mice fed fish oil or the PPAR
ligand. In the same mice, expression of the lipolytic gene, hormone-sensitive lipase was increased (P < 0.05). Fish oil feeding also stimulated expression of genes participating in fatty acid oxidation in the liver of transgenic mice compared with wild-type mice. Overall, these results indicate that PUFA may serve as natural and effective regulators of lipid catabolism in vivo and many of these effects may be generated from activation of PPAR
. Key Words: adipose tissue • fish oil • lipid metabolism • peroxisome proliferator-activated receptor
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