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Journal of Animal Science Abstract - Animal Growth, Physiology, and Reproduction

Porcine peroxisome proliferator-activated receptor δ mediates the lipolytic effects of dietary fish oil to reduce body fat deposition1


This article in JAS

  1. Vol. 88 No. 6, p. 2009-2018
    Received: Oct 21, 2009
    Accepted: Feb 17, 2010
    Published: December 4, 2014

    3 Corresponding author(s):

  1. Y. H. Yu*,
  2. P. H. Wang*,
  3. W. T. K. Cheng,
  4. H. J. Mersmann*22,
  5. S. C. Wu 3 and
  6. S. T. Ding 3
  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



Peroxisome proliferator-activated receptor δ promotes fatty acid catabolism and energy expenditure in skeletal muscle and adipose tissues. A ligand for PPARδ is required to activate PPARδ function. Polyunsaturated fatty acids are potential ligands for PPARδ activation. The current experiment was designed to determine the potential for PUFA, particularly from dietary fish oil, to activate porcine PPARδ in vivo. Transgenic mice were generated to overexpress porcine PPARδ 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 PPARδ 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 PPARδ 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 PPARδ.

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