These results indicate that CCH impaired colonic barrier function, markedly reduced the protein levels of GPR41 and GPR43, and aggravated overexpression of HDAC1/2, which were ameliorated by FMT and SCFA treatment (Fig. 4E, F), suggesting alleviation of colonic barrier dysfunction via activation of GPR41 and GPR43 and inhibition of HDAC. Here, FFAR2 is linked to columnar cell hyperplasia of the breast.