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肥胖的胎儿起源

Fetal origins of obesity.

作者信息

Oken Emily, Gillman Matthew W

机构信息

Department of Ambulatory Care and Prevention, Harvard Medical School/Harvard Pilgrim Health Care, Boston, Massachusetts, USA.

出版信息

Obes Res. 2003 Apr;11(4):496-506. doi: 10.1038/oby.2003.69.

DOI:10.1038/oby.2003.69
PMID:12690076
Abstract

The worldwide epidemic of obesity continues unabated. Obesity is notoriously difficult to treat, and, thus, prevention is critical. A new paradigm for prevention, which evolved from the notion that environmental factors in utero may influence lifelong health, has emerged in recent years. A large number of epidemiological studies have demonstrated a direct relationship between birth weight and BMI attained in later life. Although the data are limited by lack of information on potential confounders, these associations seem robust. Possible mechanisms include lasting changes in proportions of fat and lean body mass, central nervous system appetite control, and pancreatic structure and function. Additionally, lower birth weight seems to be associated with later risk for central obesity, which also confers increased cardiovascular risk. This association may be mediated through changes in the hypothalamic pituitary axis, insulin secretion and sensing, and vascular responsiveness. The combination of lower birth weight and higher attained BMI is most strongly associated with later disease risk. We are faced with the seeming paradox of increased adiposity at both ends of the birth weight spectrum-higher BMI with higher birth weight and increased central obesity with lower birth weight. Future research on molecular genetics, intrauterine growth, growth trajectories after birth, and relationships of fat and lean mass will elucidate relationships between early life experiences and later body proportions. Prevention of obesity starting in childhood is critical and can have lifelong, perhaps multigenerational, impact.

摘要

全球肥胖流行态势持续不减。众所周知,肥胖极难治疗,因此预防至关重要。近年来,一种新的预防模式应运而生,该模式源自子宫内环境因素可能影响终身健康这一观念。大量流行病学研究表明,出生体重与日后达到的体重指数(BMI)之间存在直接关联。尽管数据因缺乏潜在混杂因素的信息而受限,但这些关联似乎很可靠。可能的机制包括脂肪和瘦体重比例的持久变化、中枢神经系统对食欲的控制以及胰腺的结构和功能。此外,较低的出生体重似乎与日后发生中心性肥胖的风险相关,而中心性肥胖也会增加心血管疾病风险。这种关联可能通过下丘脑 - 垂体轴、胰岛素分泌与感知以及血管反应性的变化来介导。较低的出生体重与较高的BMI相结合,与日后的疾病风险关联最为强烈。我们面临着出生体重谱两端肥胖增加这一看似矛盾的现象——出生体重较高时BMI较高,出生体重较低时中心性肥胖增加。未来关于分子遗传学、子宫内生长、出生后生长轨迹以及脂肪与瘦体重关系的研究将阐明早期生活经历与日后身体比例之间的关系。从儿童期开始预防肥胖至关重要,且可能产生终身影响,甚至可能影响多代人。

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