宫内发育迟缓与成年期高脂血症的早期防治机制
Early prevention and treatment mechanism of intrauterine growth retardation and adult hypertriglyceridemia
周来仪 1贺晓日1
作者信息
- 1. 中南大学湘雅二医院,湖南 长沙 410011
- 折叠
摘要
大量流行病学的资料证实宫内发育迟缓(intrauterine growth retardation,IUGR)与成年期代谢综合征(高血糖、高血脂、高血压等)密切相关,其机制很可能是影响组织细胞某些关键基因启动子区域如过氧化物酶体增殖物激活受体α(peroxisome proliferator-activated receptor α,PPARα)启动子区域的甲基化改变,引起PPARα异常表达,介导脂肪酸氧化分解代谢异常,导致成年期代谢综合征的发生.叶酸是体内重要的甲基供体,参与核苷酸的生物合成和甲基化,其营养状况可影响许多基因的表达.如果生命早期给予叶酸提供甲基供体,可能在一定程度上能逆转PPARα启动子区域的甲基化改变,为IUGR成年期高甘油三酯血症的早期防治提供新思路.
Abstract
Extensive epidemiological data have confirmed that intrauterine growth retardation(IUGR)is closely related to adult metabolic syndrome(including hyperglycemia,hyperlipidemia,hypertension,etc.),and its mechanism is probably going to influence the methylation of certain important tissue cell gene promoter regions like the promoter region of peroxisome proliferator-activated receptor α(PPARα),which will lead to aberrant expression of PPARα,abnormal oxidative catabolism of fatty acids,and adult metabolic syndrome.Folic acid is an essential methyl donor in the body,involved in nucleotide biosynthesis and methylation,and its nutritional status can influence the expression of several genes.Early folic acid supplementation as a methyl donor may partially undo the methylation alterations in the PPARα promoter region,offering a novel approach to the early prevention and treatment of hypertriglyceridemia in adult IUGR patients.
关键词
宫内发育迟缓/高甘油三脂血症/过氧化物酶体增殖物激活受体α/DNA甲基化/营养早期干预Key words
intrauterine growth retardation/hypertriglyceridemia/peroxisome proliferator-activated receptor α/DNA methylation/early nutritional intervention引用本文复制引用
基金项目
湖南省自然科学基金项目(2020JJ4785)
澳优食品与营养科学研究基金项目(AU-YJY-B-LX-20-022)
出版年
2024
NETL
NSTL
万方数据