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糖尿病的发生是遗传和环境因素共同作用的结果。近年来,人们开始关注生命早期发育状况对成年期疾病的影响。越来越多证据显示,宫内不良发育环境(IUGR)导致成年期糖代谢异常可能是通过表观遗传机制发挥作用的,如通过基因的甲基化修饰、组蛋白密码影响基因的表达,此遗传倾向最终导致后代临床表型变化。不良宫内发育环境(IUGR)模型鼠研究显示,在胰岛、肝脏和骨骼肌组织中与糖代谢相关的基因均发生了表观遗传修饰改变,导致相应组织基因表达异常,增加了糖代谢异常发生风险。
The onset of diabetes is the result of a combination of genetic and environmental factors. In recent years, people began to pay attention to the impact of early life conditions on adult diseases. There is growing evidence that IUGR causes abnormal glucose metabolism in adulthood possibly through epigenetic mechanisms such as methylation of genes and histone codons affecting gene expression, Genetic predisposition ultimately leads to clinical phenotypic changes in offspring. In intrauterine developmental environment (IUGR) model mice, studies have shown that in the islet, liver and skeletal muscle genes related to glucose metabolism have occurred epigenetic modification changes, resulting in abnormal gene expression of the corresponding tissue, an increase of abnormal glucose metabolism risk.