The activation of bile acid receptors, including FXR and takeda G protein-coupled receptor 5 (TGR5) which increase FAO are promising therapeutic targets for CKD.155 FXR agonist GW4064 decreased glomerulosclerosis and interstitial fibrosis by inhibiting the SREBP1 expression.156 Selective FXR agonist INT-747 modulated lipid accumulation and improved renal injury, such as proteinuria, glomerulosclerosis, and tubulointerstitial fibrosis in streptozotocin (STZ)-induced DN mice.70 The possible mechanism might be inhibiting the transcriptional activity of NF-κB. This evidence concerns the gene GPBAR1 and glomerulosclerosis.