Intestinal regulation of urinary sodium excretion and the pathophysiology of diabetic kidney disease: a focus on glucagon‐like peptide 1 and dipeptidyl peptidase 4

摘要: The tubular hypothesis of glomerular filtration and nephropathy in diabetes is a pathophysiological concept that assigns critical role to the system, including proximal hyperreabsorption growth, which relevant for early hyperfiltration later chronic kidney disease. Here we focus on how harnessing bioactivity hormones released from gut may ameliorate effects part by attenuating growth. endogenous tone glucagon-like peptide 1 (GLP-1)/GLP-1 receptor (GLP-1R) system its pharmacologic activation are nephroprotective independent changes blood glucose. This associated with suppression increases weight hyperfiltration, reflect at least inhibitory Inhibition dipeptidyl peptidase 4 (DPP-4) also glucose involves GLP-1/GLP-1R dependent mechanisms. GLP-1R agonist exendin-4 induces natriuresis via GLP-1R. In contrast, DPP4 inhibition, albeit circulating GLP-1, drives natriuretic response implying other DPP-4 substrates. extent intrarenal DPP-4/GLP-1 contributes all these remains be established as does direct impact renal inflammation.