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胰高血糖素样肽1受体激动剂对代谢相关脂肪性肝病作用机制的研究进展 被引量:2

Update on glucagon-like peptide-1 receptor agonists in metabolic associated fatty liver disease
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摘要 非酒精性脂肪性肝病(NAFLD)(现已更名为代谢相关脂肪性肝病)是一种以肝实质内脂质过度沉积为特征,常与中心性肥胖、2型糖尿病、胰岛素抵抗、代谢综合征等疾病合并存在,被认为是代谢综合征的肝脏表现。非酒精性脂肪性肝炎(NASH)是一种可能导致肝硬化、肝细胞癌的进行性肝病。目前尚无批准用于治疗NAFLD/NASH的药物。近期研究表明胰高血糖素样肽1(GLP-1)受体激动剂作为降糖药,不仅通过肠促胰素作用改善代谢关键参数间接逆转NAFLD的进展,还直接影响肝细胞脂质代谢、炎症及氧化应激。文章对GLP-1受体激动剂在NAFLD/NASH中的作用及潜在机制进行综述。 Nonalcoholic fatty liver disease(NAFLD)is characterized by excessive lipid deposition within the liver parenchyma,and is usually accompanied with obesity,insulin resistance,type 2 diabetes(T2DM),insulin resistance,metabolic syndrome.Recently,NAFLD has been officially renamed metabolic associated fatty liver disease(MAFLD).Nonalcoholic steatohepatitis(NASH)is a progressive liver disease that can lead to cirrhosis,hepatocellular carcinoma.Currently there are no approved drugs available for NAFLD/NASH treatment.Glucagon-like peptide-1(GLP-1)receptor agonist not only reverses the progression of NAFLD indirectly through an incretin effect that improves key metabolic parameters involved in NAFLD,but also has a direct effect on lipid metabolism,inflammation and oxidative stress of hepatocytes.Herein,this study reviews the effects and potential mechanisms of GLP-1 receptor agonists on nonalcoholic fatty liver disease.
作者 李娜 刘佳 王广 谢国敏 曲爱娟 李红梅 LI Na;LIU Jia;WANG Guang;XIE Guomin;QU Aijuan;LI Hongmei(Department of Endocrinology,Beijing Chaoyang Hospital Affiliated to Capital Medical University,Beijing 100020,C hina;Department of Endocrinology,the First Affiliated Hospital of Tsinghua University,Beijing 100016,China;Department of Physiology and Pathophysiology,School of Basic Medical Sciences&Key Laboratory of Remodeling-Related Cardiovascular Diseases,Ministry of Education,Capital Medical University,Beijing 100069,China)
出处 《中国动脉硬化杂志》 CAS 2021年第5期446-450,共5页 Chinese Journal of Arteriosclerosis
基金 国家自然科学基金面上项目(81770792) 北京市自然科学基金B类重点项目(KZ201810025038)。
关键词 代谢相关脂肪性肝病 胰高血糖素样肽1受体激动剂 脂质代谢 自噬 炎症 氧化应激 metabolic associated fatty liver disease GLP-1 receptor agonist lipid metabolism autophagy inflammation oxidative stress
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