Antioxidants

BACKGROUND: Excessive fructose intake causes metabolic syndrome and lipid accumulation in the kidney and leads to renal dysfunction and damage. Exercise (Ex) improves lipids regulation, but the mechanisms are remaining unclarified in the kidney.

METHODS: Male Sprague-Dawley rats were allocated to groups fed with CON or HFr diet. A part of rats in each group underwent treadmill exercise at an aerobic intensity for 12 weeks. Drug treatment was performed as the fenofibrate gavage during the last 4 weeks on HFr-fed rats. Renal function, histological changes and the expression of regulators involved in FA metabolism were assessed.

RESULTS: In CON-fed groups, Ex did not affect renal function or histology, and significantly increased the renal expression of FA b-oxidation regulators including acyl-CoA dehydrogenases (CADs), acyl-CoA oxidase (ACOX), peroxisome proliferator-activated receptorα (PPARα) and PPARγ-coactivator-1α (PGC-1α), and lipogenic factors including acetyl-CoA carboxylase (ACCα) and FA synthase (FAS), sterol regulatory element-binding protein 1c (SREBP1c). HFr caused albuminuria, lipid accumulation and renal pathohistological changes, which attenuated by Ex but not by fenofibrate. HFr decreased the renal expression of medium and short-chain CADs, PPARα, and increased the renal expression of lipogenesis enzymes including ACCα, FAS, and SREBP1c. Ex increased the expression of CADs, carnitine palmitoyltransferase type I (CPT-I), ACOX, PPARα, and PGC-1α anddecreased the expression of ACCα, FAS in the HFr-fed rats. The Ex-induced FA metabolism alteration was similar to those in the fenofibrate-treated group.

CONCLUSION: present study indicated that Ex enhances renal FA metabolism, which might protect the kidney in the lipids dysregulation diseases.