Obesity and Gestational Diabetes Mellitus Pathways for Programming in Mouse, Monkey, and Man—Where Do We Go Next? The 2014 Norbert Freinkel Award Lecture.
Obesity and Gestational Diabetes Mellitus Pathways for Programming in Mouse, Monkey, and Man—Where Do We Go Next? The 2014 Norbert Freinkel Award Lecture.
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DOI：
10.2337/dc15-0628
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发表时间：
2015-08
期刊：
影响因子：
16.2
通讯作者：
Friedman JE
中科院分区：
文献类型：
--
作者：
Friedman JE
肥胖和妊娠期糖尿病在全球范围内持续增加，并且跨越年龄、种族、民族和社会经济地位的范围。令人担忧的是，十分之一的婴儿和幼儿肥胖，五分之一的青年既肥胖又有青春期前代谢综合征的风险。母亲健康状况不佳如何给后代带来未来代谢疾病风险的潜在机制开始在人类和非人类灵长类动物模型中出现。母亲的饮食和肥胖会影响燃料、激素和炎症，对胎儿的代谢系统产生强大的影响。这些伴随着婴儿微生物组和表观基因组以及后代行为的持续变化。这些结果表明，妊娠期和哺乳期的饮食暴露正在推动下一代的健康风险。母亲的饮食是否可以防止子宫内的变化，从而改变婴儿生命过程中的疾病风险，仍然是未知的。为了更健康的下一代，迫切需要进行有控制的、机械的研究来确定干预措施。
Obesity and gestational diabetes mellitus continue to increase worldwide and span the spectrum of age, race, ethnicity, and socioeconomic status. Alarmingly, 1 in 10 infants and toddlers is obese, and 1 in 5 youths is both obese and at risk for metabolic syndrome prior to puberty. The mechanisms underlying how poor maternal health imparts risk for future metabolic disease in the offspring are beginning to emerge in deeply phenotyped human and nonhuman primate models. Maternal diet and obesity impact fuels, hormones, and inflammation with powerful effects on fetal metabolic systems. These are accompanied by persistent changes in the infant microbiome and epigenome and in offspring behavior. These results suggest that gestational and lactational dietary exposures are driving health risks in the next generation. Whether maternal diet can prevent changes in the womb to alter infant life-course disease risk is still unknown. Controlled, mechanistic studies to identify interventions are sorely needed for a healthier next generation.