高血糖介导的卵母细胞 TET3 不足使后代易患葡萄糖不耐受。

Hyperglycemia-mediated oocyte TET3 insufficiency predisposes offspring to glucose intolerance.

机构信息

Department of Endocrinology and Metabolism, Guangdong Provincial Key Laboratory of Diabetology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.

Division of Life Sciences and Medicine, Department of Endocrinology, Institute of Endocrine and Metabolic Diseases, The First Affiliated Hospital of USTC, Clinical Research Hospital of Chinese Academy of Sciences (Hefei), University of Science and Technology of China, Hefei, China.

出版信息

J Diabetes Investig. 2022 Oct;13(10):1649-1651. doi: 10.1111/jdi.13885. Epub 2022 Jul 29.

DOI:10.1111/jdi.13885

PMID:35839128

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9533033/

Abstract

In a recent article published in Nature, Chen et al. reported that pregestational hyperglycemia rendered offspring vulnerable to glucose intolerance due to insufficient TET3-mediated 5-methylcytosine oxidation and DNA demethylation, resulting in hypermethylation and reduction of insulin-secreting genes.

摘要

在最近发表在《自然》杂志上的一篇文章中，Chen 等人报道称，孕前高血糖使后代易患葡萄糖不耐受，原因是 TET3 介导的 5-甲基胞嘧啶氧化和 DNA 去甲基化不足，导致胰岛素分泌基因的过度甲基化和减少。