首页|艾塞那肽改善T2DM患者和db/db小鼠肝脏胰岛素抵抗的作用

艾塞那肽改善T2DM患者和db/db小鼠肝脏胰岛素抵抗的作用

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目的:探讨艾塞那肽对肝胰岛素抵抗(IR)的作用。方法:选取2017年8月~2020年8月连续使用艾塞那肽治疗6个月的80例T2DM患者,检测患者用药前后糖化血红蛋白(HbA1c)、空腹血糖(FPG)等指标,计算体质量指数(BMI)、稳态模型胰岛素抵抗指数(HOMA-IR)与稳态模型胰岛功能(HOMA-β)。以db/db小鼠为糖尿病研究模型,艾塞那肽连续治疗8周,进行葡萄糖耐受(OGTT)和胰岛素耐受(ITT)试验,测定FPG和胰岛素水平;肝脏切片进行HE和PAS染色。结果:艾塞那肽治疗后,T2DM患者HbA1c、FPG、HOMA-IR水平明显降低(P<0。05);艾塞那肽增加HepG2细胞IR模型的萄萄糖消耗量(P<0。05);艾塞那肽降低db/db小鼠FPG、空腹血清胰岛素、HOMA-IR,胰岛素敏感性增加,肝糖原累积面积增加(P<0。05)。结论:艾塞那肽可显著改善肝胰岛素抵抗。
Effects of Exenatide on Hepatic Insulin Resistance in T2DM Patients and db/db Mice
Objective:To investigate the effects of exenatide on hepatic insulin resistance(IR),which provides a strong basis for the treatment of hepatic insulin resistance in type 2 diabetes mellitus(T2DM).Methods:A total of 80 patients with T2DM that were treated with exenatide for 6 months from August 2017 to August 2020 were enrolled.Glycosylated hemoglobin(HbA1c)and fasting blood glucose(FPG)were measured before and after treatment,moreover,body mass index(BMI),homeostatic model insulin re-sistance index(HOMA-IR)and homeostatic model islet function(HOMA-β)were calculated.The db/db mice were treated with exenatide for 8 weeks,OGTT andi ITT experiments were performed,and then fasting blood glucose and insulin levels were determined,liver sections were stained with HE and PAS.Results:After treatment of exenatide,the levels of HbA1c,FPG and HOMA-IR were significantly decreased in T2DM(P<0.05).Exenatide increased glucose consumption in IR model of HepG2 cells(P<0.05);Exe-natide decreased fasting blood glucose,fasting serum insulin(FINS)and HOMA-IR in db/db mice,in-creased insulin sensitivity index(ISI)and liver glycogen accumulation area(P<0.05).Conclusion:Exe-natide improves hepatic insulin resistance.

Type 2 diabetes mellitusInsulin resistanceExenatide

秦亚玮、李娜、黄钰涵、王晓彤、凌宏威、王涛

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徐州医科大学附属医院药学部,徐州 221006

徐州医科大学附属医院内分泌科,徐州 221006

2型糖尿病 胰岛素抵抗 艾塞那肽

国家自然科学基金江苏省研究型医院学会-精益化用药-石药专项科研基金徐州市卫生健康委彭城英才医学青年后备人才项目

82003866JY202201XWRCHT20220034

2024

药学与临床研究
江苏省药学会

药学与临床研究

CSTPCD
影响因子:0.95
ISSN:1673-7806
年,卷(期):2024.32(2)
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