TRAF6 and type 2 diabetes mellitus: The in vitro study of colonic epithelial cells showed that the over-expression of NLRC3 potentially benefited colonic epithelial barrier integrity due to the increase of TNF receptor-associated factor 6 (TRAF6)-mediated ZO-1 and occludin expression, and butyrate could improve the intestinal barrier in type 2 diabetic mice by upregulating GPR43 expression and stimulating NLCR3 in a TRAF6-dependent manner [88].