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首页> 外文期刊>Journal of cellular physiology. >Dapaglif lozin ameliorates pancreatic injury and activates kidney autophagy by modulating the AMPK/mTOR signaling pathway in obese rats
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Dapaglif lozin ameliorates pancreatic injury and activates kidney autophagy by modulating the AMPK/mTOR signaling pathway in obese rats

机译：Dapaglif lozin改善胰腺损伤和激活肾脏自噬通过调制AMPK / mTOR信号通路在肥胖老鼠

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Chronic consumption of a high-fat diet induces obesity and impairs the ultra-structure of organs and tissues. We examined the effect of sodium-glucose cotransporter 2 (SGLT2) inhibitor-dapagliflozin on renal and pancreatic injuries in obese condition. Rats were fed a high-fat diet for 16 weeks to induce obesity. After that, dapagliflozin or vildagliptin, 1.0 or 3.0 mg/kg/day, respectively, was administered by oral gavage for 4 weeks. The effects of dapagliflozin on insulin resistance, kidney autophagy, pancreatic oxidative stress, en-doplasmic reticulum (ER) stress, inflammation, and apoptosis in high-fat diet-induced obese rats were elucidated. High-fat-diet fed rats demonstrated metabolic abnormalities including increased body weight, visceral fat weight, plasma insulin, plasma cholesterol, homeostasis model assessment (HOMA) index, and TAUCg, indicating the obese-insulin resistant and glucose intolerance conditions. Also, high-fat-diet fed rats exhibited significant pancreatic injury accompanied by decreased kidney autophagy. Dapagliflozin or vildagliptin treatment for 4 weeks ameliorated pancreatic oxidative stress, ER stress, inflammation, and apoptosis and restored kidney autophagy in obese rats. Moreover, the morphology changes of the pancreas and kidney were improved in the treated groups. Interestingly, dapagliflozin showed higher efficacy than vildagliptin in improving body weight, visceral fat weight, plasma cholesterol level, and pancreatic oxidative stress in our model. Taken together, the present study demonstrated that the therapeutic effects of dapagliflozin attenuated pancreatic injury, pancreatic oxidative stress, ER stress, inflammation, apoptosis, and exerted re no protective effects by restoring autophagic signaling in obese rats.
机译：长期食用高脂饮食诱发肥胖和损害大鼠器官和组织。sodium-glucose转运蛋白2 (SGLT2)inhibitor-dapagliflozin肾和胰腺受伤在肥胖状态。16周高脂肪饮食诱导肥胖。之后,dapagliflozin或vildagliptin 1.0或3.0毫克/公斤/天,分别是由口服填喂法为4周。dapagliflozin胰岛素抵抗,肾脏自噬,胰腺氧化应激,en-doplasmic网(ER)压力,炎症,和在高脂肪食源性肥胖大鼠细胞凋亡被阐明。证明了代谢异常包括增加体重,内脏脂肪重量,血浆胰岛素、血浆胆固醇体内平衡模型评估(HOMA)指数,TAUCg表明obese-insulin耐药葡萄糖耐受不良环境。雌性老鼠表现出显著的胰腺损伤伴有肾功能下降自噬。改善胰腺癌治疗4周氧化应激、ER应激、炎症细胞凋亡和恢复肾脏自噬在肥胖老鼠。胰腺和肾脏中改善治疗组。比vildagliptin提高更高的功效体重、内脏脂肪重量、等离子体胆固醇水平和胰腺氧化压力在我们的模型中。研究表明,治疗效果dapagliflozin减毒的胰腺损伤,胰腺氧化应激,压力,炎症、细胞凋亡和对不保护作用,恢复自噬信号在肥胖老鼠。

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