Abstract
Lifestyle improvement, including through exercise, has been recognized as an important mode of therapy for the suppression of diabetic kidney disease (DKD). However, the detailed molecular mechanisms by which exercise exerts beneficial effects in the suppression of DKD have not yet been fully elucidated. In this study, we investigate the effects of treadmill exercise training (TET) for 8 weeks (13 m/min, 30 min/day, 5 days/week) on kidney injuries of type 2 diabetic male rats with obesity (Wistar fatty (fa/fa) rats: WFRs) at 36 weeks of age. TET significantly suppressed the levels of albuminuria and urinary liver-type fatty-acid-binding protein (L-FABP), tubulointerstitial fibrosis, inflammation, and oxidative stress in the kidneys of WFRs. In addition, TET mitigated excessive apoptosis and restored autophagy in the renal cortex, as well as suppressed the development of morphological abnormalities in the mitochondria of proximal tubular cells, which were also accompanied by the restoration of AMP-activated kinase (AMPK) activity and suppression of the mechanistic target of rapamycin complex 1 (mTORC1). In conclusion, TET ameliorates diabetes-induced kidney injury in type 2 diabetic fatty rats.
Highlights
The blood glucose under ad libitum feeding and HbA1c levels were significantly elevated in the Wistar fatty (fa/fa) rats (WFRs) and WFRs-T compared with the Wistar lean (fa/+) rats (WLRs); there were no differences between the WFRs and WFRs-T (Figure 1H,I)
Levels of urinary albumin and liver-type fatty-acid-binding protein (L-FABP) excretion were markedly increased in the WFRs compared with the WLRs; these increased levels were significantly decreased with treadmill exercise training (TET), i.e., in the WFRs-TET (Figure 1J,K)
TET resulted in improvements by mitigating excessive apoptosis and restoring impaired autophagy in the renal cortex as well as mitochondrial morphology with respect to abnormalities in proximal tubular cells, which were accompanied by AMPK activation and mechanistic target of rapamycin complex 1 (mTORC1) suppression
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The number of patients with type 2 diabetes mellitus (T2DM) has been increasing worldwide. Vascular complications due to diabetes include microvascular disorders, including retinopathy, neuropathy, and kidney disease, and macrovascular disorders caused by atherosclerosis [1]. Diabetic kidney disease (DKD) occurs in approximately 30–40% of diabetic patients and is still the leading cause of end-stage kidney disease (ESKD) [2]. Establishing effective treatments for DKD, in order to preserve kidney function, is necessary. The well-recognized pathogenesis of DKD includes increased hyperglycemia, along with chronic inflammation and oxidative stress [3,4]
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