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胎盘、母体饮食与新生儿脂肪组织发育

The Placenta, Maternal Diet and Adipose Tissue Development in the Newborn.

作者信息

Symonds Michael E, Bloor Ian, Ojha Shalini, Budge Helen

机构信息

Early Life Research Unit, Academic Division of Child Health, Obstetrics and Gynaecology, The University of Nottingham, Nottingham, UK.

出版信息

Ann Nutr Metab. 2017;70(3):232-235. doi: 10.1159/000464301. Epub 2017 Mar 17.

DOI:10.1159/000464301
PMID:28301844
Abstract

BACKGROUND

A majority of adipose tissue present in the newborn possess the unique mitochondrial protein, uncoupling protein (UCP1). It is thus highly metabolically active and capable of producing 300 times more heat per unit mass than any other organ in the body. The extent to which maternal obesity and/or an obesogenic diet impacts on placental function thereby resetting the relative distribution of different types of fat in the fetus is unknown.

SUMMARY

Developmentally the majority (if not all) fat in the fetus can be considered as classical brown fat, in which UCP1 is highly abundant. In contrast, beige (or recruitable) fat which possess 90% less UCP1 may only appear after birth, as a majority of fat depots undergo a pronounced transformation that is usually accompanied by the loss of UCP1. The extent to which this process can be modulated in a depot-specific manner and/or changes in the maternal metabolic environment remain unknown. Key Messages: An increased understanding of the mechanism by which offspring born to mothers possess excessive adipose tissue could enable sustainable interventions designed to promote the abundance of UCP1 possessing adipocytes. Ultimately, this would increase their energy expenditure and improve glucose homeostasis in these individuals.

摘要

背景

新生儿体内的大部分脂肪组织含有独特的线粒体蛋白——解偶联蛋白(UCP1)。因此,它具有很高的代谢活性,每单位质量产生的热量比身体其他任何器官多300倍。母体肥胖和/或致胖饮食对胎盘功能的影响程度,从而重新设定胎儿体内不同类型脂肪的相对分布情况尚不清楚。

总结

从发育角度来看,胎儿体内的大部分(如果不是全部)脂肪可被视为典型的棕色脂肪,其中UCP1含量很高。相比之下,UCP1含量少90%的米色(或可诱导)脂肪可能只在出生后出现,因为大多数脂肪库会经历显著的转变,通常伴随着UCP1的丧失。这个过程在多大程度上可以以特定脂肪库的方式进行调节和/或母体代谢环境的变化仍不清楚。关键信息:深入了解母亲所生后代脂肪组织过多的机制,可能有助于制定可持续的干预措施,以促进含有UCP1的脂肪细胞的数量。最终,这将增加这些个体的能量消耗并改善葡萄糖稳态。

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