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2型糖尿病的宫内起源

Intra-uterine origins of type 2 diabetes.

作者信息

Jones R Huw, Ozanne Susan E

机构信息

Department of Clinical Biochemistry, Addenbrookes Hospital, University of Cambridge, Cambridge, UK.

出版信息

Arch Physiol Biochem. 2007 Feb;113(1):25-9. doi: 10.1080/13813450701318484.

Abstract

Epidemiological studies have linked low birth weight with an increased risk of type 2 diabetes in later life. This finding has been observed in many populations worldwide, in many different ethnic and socio-economic groups. These studies led to the proposal of the 'thrifty phenotype hypothesis' that suggests that the foetal environment plays a major role in mediating this relationship. Here we review the human studies and those in animal models which support the 'thrifty phenotype hypothesis'. Molecular pathways underlying the mechanisms by which a suboptimal foetal environment leads to increased risk of type 2 diabetes are discussed, along with future directions outlining how these pathways and programming events can be further dissected to discover plausible intervention strategies to reduce type 2 diabetes.

摘要

流行病学研究表明,低出生体重与日后患2型糖尿病的风险增加有关。这一发现已在全球许多人群、许多不同种族和社会经济群体中得到观察。这些研究促使人们提出了“节俭表型假说”,该假说认为胎儿环境在介导这种关系中起主要作用。在此,我们回顾支持“节俭表型假说”的人体研究和动物模型研究。我们将讨论胎儿环境欠佳导致2型糖尿病风险增加的潜在分子途径,以及未来的研究方向,概述如何进一步剖析这些途径和程序化事件,以发现合理的干预策略来降低2型糖尿病的发病率。

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