Early determinants of type-2 diabetes

Early determinants of type-2 diabetes
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DOI:
10.1016/j.beem.2012.03.002
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发表时间:
2012-10-01
影响因子:
7.4
通讯作者:
Ozanne, S. E.
Ozanne, S. E.
中科院分区:
医学2区
文献类型:
--
作者:
Berends, L. M.;Ozanne, S. E.

文献摘要

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2型糖尿病(T2 D)的全球患病率在过去30年中增加了一倍多,预计将继续以惊人的速度上升。相关的健康和经济负担相当大。T2 D常见形式的病因是多因素的,涉及遗传、表观遗传和环境因素之间复杂的相互作用。环境,特别是我们的饮食和久坐的生活方式,在糖尿病风险中的影响作用是众所周知的。主要关注的是儿童中早发性T2 D或糖尿病前期特征的患病率增加。近年来,早期生活环境在规划糖尿病风险中的作用一直是许多人类和动物研究的焦点。历史研究强调了低出生体重与成年糖尿病风险之间的关联,低出生体重是子宫内发育不佳的代表。近年来,很明显,各种暴露,包括母亲肥胖和/或母亲糖尿病,可以对后代的健康结果产生显着影响。更复杂的是,T2 D的父系和跨代传播可能发生,从而介导了代际之间疾病风险的永久循环。必须阐明基本机制,以便采取干预措施。在这样做的过程中,有可能预防、延迟或逆转由产前和/或产后环境因素诱导的T2 D的预编程风险,以改善健康结果并抑制过早的代谢下降。本综述提供了早期生活环境如何编程T2 D风险的证据,并提出了可能发生这种情况的一些机制。(c)2012爱思唯尔有限公司保留所有权利。
The global prevalence of type-2 diabetes (T2D) has more than doubled in the last 30 years and is predicted to continue to rise at an alarming rate. The associated health and financial burdens are considerable. The aetiology of common forms of T2D is multifactorial and involves a complex interplay between genetic, epigenetic and environmental factors. The influential role of the environment, in particular our diet and sedentary lifestyles, in diabetes risk is well established. Of major concern is the increasing prevalence of early onset T2D or pre-diabetic characteristics in children. In recent years, the role of the early life environment in programming diabetes risk has been the focus of numerous human and animal studies. Historical studies highlighted an association between low birth-weight, a proxy for suboptimal in utero growth, and diabetes risk in adulthood. Over more recent years it has become apparent that a variety of expositions, including maternal obesity and/or maternal diabetes, can have a significant effect on offspring health outcomes. Further complicating matters, paternal and transgenerational transmission of T2D can occur thus mediating a perpetuating cycle of disease risk between generations. It is imperative for the underlying mechanisms to be elucidated so that interventions can be introduced. In doing so, it may be possible to prevent, delay or reverse a pre-programmed risk for T2D induced by pre- and/or postnatal environmental factors to improve health outcomes and curb premature metabolic decline. This review presents evidence for how the early life environment may programme T2D risk and suggests some mechanisms by which this may occur. (c) 2012 Elsevier Ltd. All rights reserved.