Monno Itaru, Ogura Yoshio, Xu Jing, Koya Daisuke, Kitada Munehiro
Department of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada 920-0293, Ishikawa, Japan.
Division of Anticipatory Molecular Food Science and Technology, Medical Research Institute, Kanazawa Medical University, Uchinada 920-0293, Ishikawa, Japan.
Antioxidants (Basel). 2021 Nov 3;10(11):1754. doi: 10.3390/antiox10111754.
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.
包括通过运动在内的生活方式改善，已被公认为是抑制糖尿病肾病（DKD）的一种重要治疗方式。然而，运动在抑制DKD中发挥有益作用的详细分子机制尚未完全阐明。在本研究中，我们调查了对36周龄的肥胖2型糖尿病雄性大鼠（Wistar肥胖（fa/fa）大鼠：WFRs）进行8周的跑步机运动训练（TET）（13米/分钟，每天30分钟，每周5天）对其肾脏损伤的影响。TET显著抑制了WFRs肾脏中的蛋白尿水平、尿肝型脂肪酸结合蛋白（L-FABP）水平、肾小管间质纤维化、炎症和氧化应激。此外，TET减轻了肾皮质中过度的细胞凋亡并恢复了自噬，还抑制了近端肾小管细胞线粒体形态异常的发展，这也伴随着AMP激活的蛋白激酶（AMPK）活性的恢复和雷帕霉素复合物1（mTORC1）机制靶点的抑制。总之，TET改善了2型糖尿病肥胖大鼠的糖尿病诱导的肾脏损伤。
