Brigitte Reusens, Nicolas Theys, Claude Remacle, Laboratory of Cell Biology, Institute of Life Science, Université Catholique de Louvain, 1348 Louvain-la-Neuve, Belgium.
World J Diabetes. 2011 Sep 15;2(9):149-57. doi: 10.4239/wjd.v2.i9.149.
Under-nutrition as well as over-nutrition during pregnancy has been associated with the development of adult diseases such as diabetes and obesity. Both epigenetic modifications and programming of the mitochondrial function have been recently proposed to explain how altered intrauterine metabolic environment may produce such a phenotype. This review aims to report data reported in several animal models of fetal malnutrition due to maternal low protein or low calorie diet, high fat diet as well as reduction in placental blood flow. We focus our overview on the β cell. We highlight that, notwithstanding early nutritional events, mitochondrial dysfunctions resulting from different alteration by diet or gender are programmed. This may explain the higher propensity to develop obesity and diabetes in later life.
孕期营养不良和营养过剩都与成人疾病（如糖尿病和肥胖症）的发生有关。最近提出了表观遗传修饰和线粒体功能编程，以解释宫内代谢环境的改变如何产生这种表型。这篇综述旨在报告由于母体低蛋白或低热量饮食、高脂肪饮食以及胎盘血流量减少导致胎儿营养不良的几种动物模型中报告的数据。我们重点关注β细胞。我们强调，尽管有早期的营养事件，但饮食或性别引起的不同变化导致的线粒体功能障碍是可被编程的。这可能解释了为什么在以后的生活中更容易患上肥胖症和糖尿病。
