Docosahexaenoic acid-rich fish oil prevented insulin resistance by modulating gut microbiome and promoting colonic peptide YY expression in diet-induced obesity mice

It is unclear how docosahexaenoic acid (DHA) improves insulin resistance via modulating gut microbiome in obese individuals. We used diet-induced obesity (DIO) mice as a model to study the effects of DHA-rich fish oil (DHA-FO) on host metabolic disorders and colonic microbiome. DHA-FO reduced fat deposition, regulated lipid profiles and alleviated insulin resistance in DIO mice. Probably because DHA-FO prevented the permeation of lipopolysaccharide across intestinal epithelial barrier, and promoted peptide YY (PYY) secretion via the mediation of short chain fatty acids receptor (FFAR2) in colon. Furthermore, DHA-FO might regulate PYY expression by reversing microbial dysbiosis, including increasing the abundance of Akkermansia muciniphila and Lactobacillus, and suppressing the growth of Helicobacter. DHA-FO also altered gut microbial function (e.g. linoleic acid metabolism) associated with PYY expression (r > 0.80, P < 0.05). Herein, DHA-FO enhanced insulin action on glucose metabolism by altering gut microbiome and facilitating colonic PYY expression in DIO mice. (C) 2021 Beijing Academy of Food Sciences. Publishing services by Elsevier B.V. on behalf of KeAi Communications Co., Ltd.

Automated summary

It is unclear how docosahexaenoic acid (DHA) improves insulin resistance via modulating gut microbiome in obese individuals. This study used a diet-induced obesity (DIO) mouse model to investigate the effects of DHA-rich fish oil (DHA-FO) on metabolic disorders and colonic microbiome. The results showed that DHA-FO reduced fat deposition, regulated lipid profiles, and alleviated insulin resistance by preventing the permeation of lipopolysaccharide and promoting peptide YY (PYY) secretion. DHA-FO also reversed microbial dysbiosis and altered gut microbial function, which were associated with PYY expression. Overall, DHA-FO enhanced insulin action on glucose metabolism by modulating gut microbiome and facilitating colonic PYY expression in DIO mice.