Trans fatty acids (TFAs) are known to increase the risk for various metabolic syndromes. The effect of TFA on dysbiosis and intestinal inflammation, especially caused by modifying innate immunity, were evaluated. Eight-week-old C57BL6/J male mice were treated with a normal diet (ND), high saturated fatty acid high sucrose diet (HFHSD), and high TFA high sucrose diet (HTHSD) for 12 weeks (A). There was no significant difference in body weight, oral intake, liver or visceral fat weight between the HFHSD and HTHSD groups (B-E). On the other hand, the HTHSD group showed more impaired glucose tolerance than the HFHSD group (p=0.015) (F and G). Multicolor flow cytometry analysis revealed that the T-bet-positive ILC3/CD45-positive cell number ratio and the M1/M2 macrophage ratio in the small intestinal lamina propria were significantly increased in the HTHSD group (p<0.001) (H-K) and the Proteobacteria phylum were significantly increased in the HTHSD group (p<0.001) (L). The concentrations of elaidic acid in liver and serum assessed by GC/MS system were significantly higher in the HTHSD group (M and N). In RAW264.7 cells treated with palmitic acid or elaidic acid, no significant difference was observed in IL-1b positive cells, but IL-12-positive cells in elaidic acid were significantly increased (O and P). These results suggesting that TFAs cause various metabolic disorders by inducing intestinal inflammation.
T. Okamura: None. R. Bamba: None. Y. Hashimoto: None. T. Senmaru: None. M. Hamaguchi: Research Support; Spouse/Partner; AstraZeneca K. K. M. Fukui: None.
The Japan Food Chemical Research Foundation