We investigated how eicosapentaenoic acid (EPA), a key component of fish oil, affects insulin sensitivity and glucose metabolism, especially in the context of high-fat diets. The study involved male mice that either had or lacked a specific protein called Rictor, associated with a pathway known to influence cellular functions.
Our findings revealed that a diet rich in fish oil significantly enhanced glucose tolerance and insulin sensitivity in these mice. Moreover, the intake of fish oil resulted in better glucose uptake in both adipose (fat) tissues and skeletal muscle, all while reducing the liver's glucose production. This improvement was marked by lower levels of insulin in the bloodstream and an increase in the phosphorylation of a protein called Akt in the fat tissues, suggesting a key role for mTORC2 activation.
Interestingly, when the mice were fed a high-fat diet supplemented with EPA, we noticed an increase in insulin sensitivity and Akt phosphorylation, although this supplementation did not significantly improve overall glucose tolerance. This suggests that while EPA promotes insulin sensitivity via mTORC2, the enhancement of glucose tolerance observed with fish oil seems to arise from other mechanisms in the body, particularly in the muscles and liver.
Our study highlights how EPA can contribute to better metabolic health by improving how the body manages insulin and glucose, particularly for those consuming high-fat diets.