In the early DKD, BAs combine with TGR5 to improve insulin sensitivity via GLP-1, as well as activate glucosyl-induced phosphorylation through FXR-mediated signaling pathways, increase the ratio of ATP/ADP, and increase cellular oxygen consumption, while intracellular calcium ion flow induces active insulin output to the outside of the cell, resulting in maintaining insulin homeostasis in the body [59]. Here, GPBAR1 is linked to diabetic kidney disease.