SUN-300 CHRONIC EXERCISE EXERTS RENOPROTECTIVE EFFECTS THROUGH ACTIVATION OF FATTY ACID OXIDATION IN THE KIDNEY OF FRUCTOSE-FED RATS

Abstract

high-fructose (HFr) causes metabolic syndrome and renal lipid accumulation, leading to renal dysfunction. Long-term exercise (Ex) has beneficial effects against metabolic disorders, but the mechanisms have not been fully elucidated in the kidney. Present study investigated the effects of Ex on renal function and fatty acid (FA) metabolism in rats fed with HFr. Thirty-two, male Sprague-Dawley rats were fed with high-fructose or control diet (CON-Sed/HFr-Sed), and half of rats in each diet group underwent chronic treadmill exercise for 12 weeks (CON-Ex/HFr-Ex). Renal histology including glomerulosclerosis, interstitial fibrosis, podocytes injury were measured. expression of regulators in FA metabolism in the kidney were then assessed. HFr intake induced glomerulosclerosis, podocyte injury, interstitial fibrosis, and lipids accumulation in the kidney, and Ex significantly attenuated the renal histological changes in HFr-Ex group while the CON-Ex showed no changes. HFr intake increased the expression of proteins involved in FA synthesis, including FA synthase (FAS), acetyl-CoA carboxylase (ACC), and sterol regulatory element-binding protein 1c (SREBP-1c), while reducing the expression of genes involved in beta-oxidation, including very long, medium, and short-chain acyl-CoA dehydrogenase (VLCD, MCAD, and SCAD), acyl-CoA oxidase (ACOX), peroxisome proliferator-activated receptor (PPAR) alpha and PPARgamma coactivator-1α (PGC-1alpha) in the kidney. Ex decreased the expression of FAS and ACC in the HFr-Ex but increased the expression in CON-Ex. Ex increased the expression of VL/L/M/SCAD, carnitine palmitoyltransferase type I, ACOX, PPARalpha, and PGC-1alpha in both Ex groups. Ex exerts renoprotective effects with attenuation of renal histological pathogenesis and enhancement of FA oxidation.