Ipragliflozin improves mitochondrial abnormalities in renal tubules induced by a high‐fat diet

• DOI: 10.1111/jdi.12802
• Publication Date: 2018-01-20T05:46:37Z
• Authors: Susumu Takagi; Jinpeng Li; Yuta Takagaki; Munehiro Kitada; Kyoko Nitta; Toshiyuki Takasu; Keizo Kanasaki; Daisuke Koya
• Keywords: Male; 2. Zero hunger; 0303 health sciences; Articles; Thiophenes; Diet, High-Fat; Mitochondria; 3. Good health; Mice, Inbred C57BL; Mice; 03 medical and health sciences; Kidney Tubules; Glucosides; Sodium-Glucose Transporter 2; Animals; Kidney Diseases; Energy Intake; Sodium-Glucose Transporter 2 Inhibitors

Complete mechanisms of renoprotective effects sodium-glucose cotransporter 2 (SGLT2) inhibitors have not been elucidated yet. Mitochondrial biogenesis is regulated by membrane GTPases, such as optic atrophy factor 1 and mitofusion 2. Here, we investigated whether SGLT2 inhibition in mice fed with a high-fat diet (HFD) improved mitochondrial morphology restored biogenesis-related molecules.Mice were control or HFD without ipragliflozin treatment. After 16 weeks, the kidneys taken out utilized for analysis.HFD-fed treated showed increased caloric intake ate more food than HFD-fed mice. Body kidney weights, blood glucose levels altered treatment Histological analysis that, compared mice, displayed tubular vacuolation, dilatation epithelial cell detachment; ameliorated these alterations. Furthermore, ultrastructural that tubule mitochondria exhibited significant damage. Again, reversed damage to normal state, Increased urine 8-hydroxydeoxyguanosine suppressed well. In vitro experiments using HK-2 cells revealed either high palmitate levels. Suppression specific small interfering ribonucleic acid GTPase their values.SGLT2 might act directly on protect from metabolic insults regardless improvement bodyweight reduction.