In the present study, we showed that compared with GPR43, GPR41 was rarely expressed in kidney tissues and in GMCs and did not show an obvious response to diabetes-relative stimulation; SCFAs reversed the downregulation of GPR43, along with inhibition of oxidative stress and NF-κB signaling, indicating that GPR43 was critically involved in SCFA-mediated beneficial effects. Here, NFKB1 is linked to diabetes mellitus.