Endocrine disrupting chemicals and the developmental programming of adipogenesis and obesity.
Endocrine disrupting chemicals and the developmental programming of adipogenesis and obesity.
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DOI：
10.1002/bdrc.20197
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发表时间：
2011-03
期刊：
影响因子：
--
通讯作者：
Blumberg B
中科院分区：
文献类型：
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作者：
Janesick A;Blumberg B
肥胖和相关疾病是一种新兴的公共卫生流行病，特别是在美国。目前，美国34%的人口患有临床肥胖症(BMI>；30)，68%的人超重(BMI>；25)，是世界平均水平的两倍多，比日本和韩国高10倍。当能量摄入超过能量消耗时，肥胖就会发生；然而，即使在相同水平的过量卡路里输入下，个体在增加体重和积累脂肪的倾向上也存在很大差异。临床、流行病学和生物学研究表明，肥胖在很大程度上是在生命早期，包括宫内时期。环境肥胖假说认为，产前或生命早期接触某些内分泌干扰物会使暴露于环境中的个人容易增加脂肪质量和肥胖。肥胖原暴露会改变多能基质干细胞的表观基因组，使它们偏向脂肪细胞谱系，损害骨骼。因此，在生命早期暴露于致肥者的人类可能会有一个改变的干细胞隔间，这是预先编程的，走向成脂的命运。这会导致更多稳定状态的脂肪细胞数量，并可能终身挣扎以保持健康的体重，这可能会因促进不良饮食和不足锻炼的社会影响而加剧。本文就脂肪细胞的发育起源、脂肪细胞数量与肥胖的关系以及肥胖化学物质如何干扰调节脂肪细胞数量和能量平衡的高效稳态机制作一综述。
Obesity and related disorders are a burgeoning public health epidemic, particularly in the U.S. Currently 34% of the U.S. population is clinically obese (BMI > 30) and 68% are overweight (BMI > 25), more than double the worldwide average and 10-fold higher than Japan and South Korea. Obesity occurs when energy intake exceeds energy expenditure; however, individuals vary widely in their propensity to gain weight and accrue fat mass, even at identical levels of excess caloric input. Clinical, epidemiological, and biological studies show that obesity is largely programmed during early life, including the intrauterine period. The environmental obesogen hypothesis holds that prenatal or early life exposure to certain endocrine disrupting chemicals can predispose exposed individuals to increased fat mass and obesity. Obesogen exposure can alter the epigenome of multipotent stromal stem cells, biasing them toward the adipocyte lineage at the expense of bone. Hence, humans exposed to obesogens during early life might have an altered stem cell compartment, which is preprogrammed toward an adipogenic fate. This results in a higher steady state number of adipocytes and potentially a lifelong struggle to maintain a healthy weight, which can be exacerbated by societal influences that promote poor diet and inadequate exercise. This review focuses on the developmental origins of the adipocyte, the relationship between adipocyte number and obesity, and how obesogenic chemicals may interfere with the highly efficient homeostatic mechanisms regulating adipocyte number and energy balance.