As summarized in Figure 8, our study provides compelling evidence that exogenous SCFAs, especially butyrate, ameliorate hyperglycemia and insulin resistance, improve renal function, ameliorate histopathological changes, and restore high glucose-induced inflammatory damage, which is attributable to the role GPR43-β-arrestin-2 signaling plays in buffering oxidative stress and blocking NF-κB activation. This evidence concerns the gene NFKB1 and Hyperglycemia.