Sodium butyrate improves mitochondrial function and kidney tissue injury in diabetic kidney disease via the AMPK/PGC-1α pathway
Yue Yu, Yuan-Yuan Jia, LI Hong-jun
Abstract
PURPOSE: the AMPK/PGC-1α pathway. METHODS: and detect changes in the AMPK/PGC-1α signaling pathway and mitochondrial function after NaBut intervention. RESULTS: NaBut attenuated blood glucose levels and reversed increases in urine and serum levels of glucose, BUN, Ucr, TG, TC, and UAE in db/db mice. NaBut improved insulin tolerance, reversed PGC-1α and p-AMPK expression level in the kidneys of db/db mice, and improved lipid accumulation and mitochondrial function. NaBut was able to reverse the effects of elevated glucose, compound C, and siRNA-PGC on ROS and ATP levels. Additionally, it increased protein expression of PGC-1α and p-AMPK. CONCLUSION: .
Topics & Concepts
MedicineAMPKSodium butyrateKidney diseaseKidneyMitochondrionRenal functionButyrateEndocrinologyDiabetes mellitusInternal medicineDiseasePharmacologyCell biologyBiochemistryEnzymeBiologyProtein kinase AGeneFermentationMetabolism, Diabetes, and CancerChronic Kidney Disease and DiabetesAdvanced Glycation End Products research