Abstract
Excess dietary lipid generally leads to fat deposition and impaired glucose homeostasis, but consumption of fish oil (FO) alleviates many of these detrimental effects. The beneficial effects of FO are thought to be mediated largely via activation of the nuclear receptor peroxisomal-proliferator- activated receptor α (PPARα) by omega-3 polyunsaturated fatty acids and the resulting upregulation of lipid catabolism. However, pharmacological and genetic PPARα manipulations have yielded variable results. We have compared the metabolic effects of FO supplementation and the synthetic PPARα agonist Wy-14,643 (WY) in mice fed a lard-based high-fat diet. In contrast to FO, WY treatment resulted in little protection against diet-induced obesity and glucose intolerance, despite upregulating many lipid metabolic pathways. These differences were likely due to differential effects on hepatic lipid synthesis, with FO decreasing and WY amplifying hepatic lipid accumulation. Our results highlight that the beneficial metabolic effects of FO are likely mediated through multiple independent pathways.
| Originalsprog | Engelsk |
|---|---|
| Artikelnummer | 5538 |
| Tidsskrift | Scientific Reports |
| Vol/bind | 4 |
| ISSN | 2045-2322 |
| DOI | |
| Status | Udgivet - 2 jul. 2014 |
Bibliografisk note
Funding Information:This work was supported by funding from the National Health and Medical Research Council of Australia (NHMRC). ML is supported by a University International Postgraduate Award from the University of New South Wales. BO is supported by a NHMRC PhD scholarship. MKM and GJC are supported by NHMRC research fellowships and NT is supported by an Australian Research Council Future Fellowship. We thank the Biological Testing Facility at the Garvan Institute (Sydney, Australia) for assistance with animal care.