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首页> 美国卫生研究院文献>International Journal of Endocrinology >Dipeptidyl-Peptidase 4 Inhibitor Sitagliptin Ameliorates Hepatic Insulin Resistance by Modulating Inflammation and Autophagy in ob/ob Mice
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Dipeptidyl-Peptidase 4 Inhibitor Sitagliptin Ameliorates Hepatic Insulin Resistance by Modulating Inflammation and Autophagy in ob/ob Mice

机译：Depteptidyl-Peptidase 4抑制剂西他列汀通过调节ob / ob小鼠的炎症和自噬来改善肝胰岛素抵抗

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Obesity and type 2 diabetes are the most common metabolic diseases globally. They are associated with inflammation, oxidative stress, autophagy, and insulin resistance. Sitagliptin, a dipeptidyl-peptidase 4 inhibitor, has been reported to show multiple biological activities beyond the antidiabetic property. This study was aimed at investigating the effect of sitagliptin on hepatic steatosis, insulin resistance, inflammation, and autophagy and exploring the underlying molecular mechanism. In the current study, ob/ob mice, a mouse model of genetic obesity and diabetes, were administered via gavage with sitagliptin 50 mg/kg daily for 4 weeks. Changes in glycolipid metabolism, inflammatory responses, and autophagy in the liver were evaluated. Body weight gain, lipid metabolic disorder, and hepatic steatosis as well as systemic and hepatic insulin sensitivity in ob/ob mice were significantly attenuated after sitagliptin treatment. Furthermore, sitagliptin decreased inflammatory responses by regulating macrophage M1/M2 polarization and inhibiting the activities of NF-κB and JNK. Moreover, sitagliptin increased the levels of phosphorylation of AMPK and decreased those of mTOR. This study indicates that sitagliptin significantly ameliorates the development of hepatic steatosis and insulin resistance in ob/ob mice by inhibiting inflammatory responses and activating autophagy via AMPK/mTOR signaling pathway.
机译：肥胖和2型糖尿病是全球最常见的代谢疾病。它们与炎症，氧化应激，自噬和胰岛素抵抗有关。西格列汀，一种二肽基-肽酶4抑制剂，据报道显示出超出抗糖尿病特性的多种生物活性。这项研究旨在调查西他列汀对肝脂肪变性，胰岛素抵抗，炎症和自噬的影响，并探讨其潜在的分子机制。在当前的研究中，ob / ob小鼠是遗传性肥胖和糖尿病的小鼠模型，每天通过西格列汀50μmg/ kg西格列汀的管饲法给药4周。评估了肝脏中糖脂代谢，炎症反应和自噬的变化。西他列汀治疗后，ob / ob小鼠的体重增加，脂质代谢紊乱和肝脂肪变性以及全身和肝胰岛素敏感性明显降低。此外，西他列汀通过调节巨噬细胞M1 / M2极化并抑制NF-κB和JNK的活性来降低炎症反应。此外，西他列汀增加了AMPK的磷酸化水平而降低了mTOR的磷酸化水平。这项研究表明，西他列汀通过抑制炎症反应和通过AMPK / mTOR信号通路激活自噬，可显着改善ob / ob小鼠肝脂肪变性和胰岛素抵抗。

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