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Early growth and postprandial glucose, insulin, lipid and inflammatory responses in adulthood

机译:成年早期生长和餐后葡萄糖,胰岛素,脂质和炎症反应

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Purpose of Review: Epidemiological findings suggest that prenatal and postnatal growth is associated with later health outcomes including cardiovascular disease and type 2 diabetes. It has been suggested that these associations are mediated through classical risk factors, for example dyslipidemia. Despite extensive epidemiological investigations, only limited data are available on the long-term influences of early growth on postprandial responses, although postprandial levels of many risk factors have been proposed to be more important than fasting levels in disease process. This review focuses on recent studies evaluating the effect of early growth on postprandial responses. Recent Findings: Current evidence from postprandial studies shows that individuals who were small at birth or grew slowly during infancy have elevated postprandial insulin and triglyceride responses. However, early growth does not seem to affect postprandial inflammatory markers. It is likely that both liver programming and abnormalities in insulin-sensitive tissues play key roles in explaining these elevated responses. Summary: Recent studies suggest that slow growth during early life has an adverse effect on postprandial metabolism, and predicts higher insulin and triglyceride responses. These elevated postprandial responses might be one underlying mechanism explaining the increased risk of cardiovascular disease and type 2 diabetes associated with nonoptimal early growth.
机译:审查目的:流行病学调查结果表明,产前和产后生长与后来的健康状况有关,包括心血管疾病和2型糖尿病。已经提出这些联系是通过经典的危险因素例如血脂异常来介导的。尽管进行了广泛的流行病学调查,但对于早期生长对餐后反应的长期影响,只有有限的数据可用,尽管已提出许多危险因素的餐后水平在疾病过程中比禁食水平更重要。这篇综述着重于评估早期生长对餐后反应影响的最新研究。最新发现:餐后研究的最新证据表明,出生时很小或婴儿期生长缓慢的个体餐后胰岛素和甘油三酸酯反应升高。但是,早期生长似乎并不影响餐后炎症指标。肝脏程序化和胰岛素敏感性组织异常可能在解释这些升高的反应中起关键作用。简介:最近的研究表明,生命早期的缓慢生长对餐后代谢产生不利影响,并预测胰岛素和甘油三酸酯反应会更高。这些升高的餐后反应可能是解释心血管疾病和与非理想早期生长相关的2型糖尿病风险增加的潜在机制之一。

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