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发育源性代谢综合征的碳水化合物母体营养过剩。

Parental overnutrition by carbohydrates in developmental origins of metabolic syndrome.

机构信息

Institute of Biology and Medical Genetics, the First Faculty of Medicine, Charles University and the General University Hospital, Prague, Czech Republic.

出版信息

Physiol Res. 2021 Dec 30;70(Suppl4):S585-S596. doi: 10.33549/physiolres.934806.

Abstract

Metabolic syndrome is a prevalent disease resulting from an interplay of genomic component and the exposome. Parental diet has been shown to affect offspring metabolic health via multiple epigenetic mechanisms. Excess carbohydrate intake is one of the driving forces of the obesity and metabolic syndrome pandemics. This review summarizes the evidence for the effects of maternal carbohydrate (fructose, sucrose, glucose) overnutrition on the modulation of metabolic syndrome components in the offspring. Despite substantial discrepancies in experimental design, common effects of maternal carbohydrate overnutrition include increased body weight and hepatic lipid content of the "programmed" offspring. However, the administration of sucrose to several rat models leads to apparently favorable metabolic outcomes. Moreover, there is evidence for the role of genomic background in modulating the metabolic programming effect in the form of nutri-epigenomic interaction. Comprehensive, robust studies are needed to resolve the temporal, sex-specific, genetic, epigenetic and nutritional aspects of parental overnutrition in the intergenerational and transgenerational pathogenesis of metabolic syndrome.

摘要

代谢综合征是一种由基因组成分和外显子组相互作用引起的常见疾病。父母的饮食已被证明通过多种表观遗传机制影响后代的代谢健康。过量摄入碳水化合物是肥胖和代谢综合征流行的主要驱动因素之一。这篇综述总结了母体碳水化合物(果糖、蔗糖、葡萄糖)营养过剩对后代代谢综合征成分调节的影响。尽管实验设计存在很大差异,但母体碳水化合物营养过剩的共同影响包括“编程”后代体重增加和肝脏脂质含量增加。然而,给几种大鼠模型喂食蔗糖会导致明显有利的代谢结果。此外,有证据表明,基因组背景在调节营养-表观遗传相互作用形式的代谢编程效应方面发挥了作用。需要进行全面、稳健的研究,以解决代谢综合征代际和跨代发病机制中父母营养过剩的时间、性别特异性、遗传、表观遗传和营养方面的问题。

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