BackgroundFish oil is known to improve lifestyle-related diseases. These effects occur partly via activation of PPARs by the n-3 polyunsaturated fatty acids included abundantly in fish oil. We investigated fish oil functions on glucose and lipid metabolism that are both dependent on and independent of PPARs pathway.MethodsMice were fed a diet containing 30 en% beef tallow (B diet) for twelve weeks to induce obesity. The mice were then divided into two groups which were fed either a B diet or a diet containing 30 en% fish oil (F diet). Each group was further divided into two groups which were administered PPARα and γ antagonists or vehicle once a day for three weeks.ResultsThe F diet groups showed lower triglyceride levels in plasma and liver than the B diet groups, but PPARs antagonists did not affect the triglyceride levels in either diet groups. The F diet groups also showed improvement of glucose tolerance compared with the B diet groups. However, PPARs antagonists made glucose tolerance worse in the F diet group but improved it in the B diet group. Therefore, by the administration of antagonists, glucose tolerance was inversely regulated between the B and F diets, and hypolipidemic action in the plasma and liver of the F diet group was not affected.ConclusionThese results suggest that fish oil decreases lipid levels in plasma and liver via PPARs pathway-independent mechanism, and that glucose tolerance is inversely regulated by PPARs antagonists under diets containing different oils.

No abstract

No abstract

The components bringing the effects of fish oil on glucose and lipid metabolism are unclear. We used hydrogenated fish oil, which has saturated fatty acids with the same carbon chain lengths as the unsaturated fatty acids in fish oil, to clarify the functions of these unsaturated fatty acids on the improvements in lipid and glucose metabolism in mice. Mice divided into 3 groups were fed different diets: fish oil diet (FO), hydrogenated fish oil diet (HFO), and soybean oil diet (SBO) as a control. Body weight gain and white adipose tissue weight in the HFO and FO groups were significantly decreased compared with those in the SBO group. However, in the HFO group, the triglyceride (TG) levels in plasma were significantly decreased, while the lipids levels in the liver were remarkably increased compared with those in the FO group. Regarding the fatty acid composition in the liver and white adipose tissue in the HFO group, in parallel with the up-regulation of stearoyl-CoA desaturase 1 mRNA, relative amounts of C16 : 1 and C18 : 1 were significantly increased. By contrast, blood glucose levels in the oral glucose tolerance test had not deteriorated in the HFO group. Our results indicate that unsaturated fatty acids in the FO diet decrease lipid levels in the liver and maintain the balance of lipid levels in plasma, liver and white adipose tissue; in addition, in the HFO group, C16 : 1 and C18 : 1 synthesized in the liver and white adipose tissue may improve glucose tolerance and lipid metabolism.

No abstract