Fetal programming of glucose-insulin metabolism

被引：76

作者：

Jones, R. Huw ^{[1
]}

Ozanne, Susan E. ^{[1
]}

机构：

[1] Univ Cambridge, Addenbrookes Hosp, Metab Res Labs, Inst Metab Sci, Cambridge CB2 0QQ, England

来源：

MOLECULAR AND CELLULAR ENDOCRINOLOGY | 2009年 / 297卷 / 1-2期

基金：

英国生物技术与生命科学研究理事会;

关键词：

Type; 2; diabetes; Programming; Beta cell; Thrifty Phenotype Hypothesis; Low protein; PANCREATIC BETA-CELLS; LOW-BIRTH-WEIGHT; LOW-PROTEIN-DIET; INTRAUTERINE GROWTH-RETARDATION; ENZYME GENE-EXPRESSION; BODY-MASS INDEX; ENDOCRINE PANCREAS; OXIDATIVE STRESS; DIABETIC MOTHERS; ISLET CELLS;

D O I：

10.1016/j.mce.2008.06.020

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Epidemiological studies have shown a link between poor fetal growth and increased risk of developing type 2 diabetes. These observations are highly reproducible in many populations worldwide although the mechanisms behind them remain elusive. The 'Thrifty Phenotype Hypothesis' was proposed to explain the underlying causes of these relationships. Animal models of poor intrauterine nutrition have been utilised to help to define the causal factors and identify the molecular mechanisms. Programmed changes in beta cell function and insulin action have been a common feature of animal models of poor intrauterine nutrition. Fundamental underlying mechanisms are starting to emerge, including changes in the epigenotype and mitochondrial function. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

引用

页码：4 / 9

页数：6

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