宫内生长受限胎儿追赶生长的表观遗传学修饰及二甲双胍干预的研究现状  

Epigenetic modification in catching growth of intrauterine growth-restricted fetus and advances in metformin intervention

作　　者：陈超阳[1] 李若茗 田欣 马凌云[1] 周颖[1,2] 崔一民[1,2] CHEN Chao-yang;LI Ruo-ming;TIAN Xin;MA Ling-yun;ZHOU Ying;CUI Yi-min(Department of Pharmacy,Peking University First Hospital,Beijing 100034,China;Department of Pharmacy Administration and Clinical Pharmacy,School of Pharmaceutical Sciences,Peking University Health Science Center,Beijing 100191,China)

机构地区：[1]北京大学第一医院药剂科,北京100034 [2]北京大学医学部药学院药事管理与临床药学系,北京100191

出　　处：《中国临床药理学杂志》2019年第23期3154-3157,共4页The Chinese Journal of Clinical Pharmacology

基　　金：北京大学第一医院科研种子基金课题资助项目(2018SF038)

摘　　要：胎儿宫内生长受限(IUGR)多由母体在妊娠时期营养供应不足引起。由于去除了阻碍生长的不利因素,IUGR胎儿在出生后可发生追赶生长(CUG),使患儿的体重、身高达到该年龄的正常范围。CUG可促发胰岛素抵抗(IR),参与成年后的代谢综合征。CUG患儿发生的IR与其基因组的表观遗传学修饰密切相关,为此类疾病的防治提供了重要的依据。近期的研究发现,胰岛素增敏剂二甲双胍可干预CUG小鼠的IR,减少成年期代谢综合征的发生。本文对IUGR及CUG的发生机制、可能发生表观遗传学修饰的主要位点、以及二甲双胍对本类患者的药理作用等作一综述。Intrauterine growth retardation(IUGR)is caused by the lack of nutrients during pregnancy.After removing the unfavorable factors that prevent the growth of the IUGR fetus,catch-up growth(CUG)can occur,which refers to the weight and height of the IUGR children could be brought to the normal range in their age.Children with CUG can develop insulin resistance(IR),and it participates in the metabolic syndrome of adulthood.The occurrence of IR is closely related to the epigenetic modification of the genome,thus the mechanism of epigenetic modification can provide an important basis for the prevention and treatment of such situations.Studies have shown that metformin had a preferable effect on IR in CUG mice,which reduced the occurrence of adult metabolic syndrome.This article reviews the mechanism of IUGR and CUG,the main sites where epigenetic modification may occur,as well as the pharmacological effects of metformin on this class of patients.

关 键 词：二甲双胍 胰岛素抵抗 表观遗传学修饰 宫内生长受限 追赶生长 

分 类 号：R977.15[医药卫生—药品]