Department of Integrative Biology and Physiology, University of Minnesota , Minneapolis, Minnesota.
Am J Physiol Regul Integr Comp Physiol. 2018 Nov 1;315(5):R867-R878. doi: 10.1152/ajpregu.00072.2018. Epub 2018 Aug 15.
The prevalence of obesity and type 2 (T2D) diabetes is a major health concern in the United States and around the world. T2D is a complex disease characterized by pancreatic β-cell failure in association with obesity and insulin resistance in peripheral tissues. Although several genes associated with T2D have been identified, it is speculated that genetic variants account for only <10% of the risk for this disease. A strong body of data from both human epidemiological and animal studies shows that fetal nutrient factors in utero confer significant susceptibility to T2D. Numerous studies done in animals have shown that suboptimal maternal environment or placental insufficiency causes intrauterine growth restriction (IUGR) in the fetus, a critical factor known to predispose offspring to obesity and T2D, in part by causing permanent consequences in total functional β-cell mass. This review will focus on the potential contribution of the placenta in fetal programming of obesity and TD and its likely impact on pancreatic β-cell development and growth.
肥胖症和 2 型糖尿病（T2D）的流行是美国和全球的主要健康关注点。T2D 是一种复杂的疾病，其特征是与肥胖和外周组织胰岛素抵抗相关的胰腺β细胞衰竭。尽管已经确定了几种与 T2D 相关的基因，但据推测，遗传变异仅占这种疾病风险的<10%。来自人类流行病学和动物研究的大量数据表明，胎儿营养因素在子宫内赋予了对 T2D 的显著易感性。许多在动物身上进行的研究表明，母体环境不佳或胎盘功能不全导致胎儿宫内生长受限（IUGR），这是一个已知的关键因素，可使后代易患肥胖症和 T2D，部分原因是导致总功能性β细胞质量的永久性后果。这篇综述将重点关注胎盘在肥胖症和 T2D 的胎儿编程中的潜在贡献及其对胰腺β细胞发育和生长的可能影响。
