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脂肪组织与胎儿编程。

Adipose tissue and fetal programming.

机构信息

The Early Life Nutrition Research Unit, Academic Division of Child Health, School of Clinical Sciences, University Hospital, Nottingham, NG7 2UH, UK.

出版信息

Diabetologia. 2012 Jun;55(6):1597-606. doi: 10.1007/s00125-012-2505-5. Epub 2012 Mar 9.

DOI:10.1007/s00125-012-2505-5
PMID:22402988
Abstract

Adipose tissue function changes with development. In the newborn, brown adipose tissue (BAT) is essential for ensuring effective adaptation to the extrauterine environment, and its growth during gestation is largely dependent on glucose supply from the mother to the fetus. The amount, location and type of adipose tissue deposited can also determine fetal glucose homeostasis. Adipose tissue first appears at around mid-gestation. Total adipose mass then increases through late gestation, when it comprises a mixture of white and brown adipocytes. BAT possesses a unique uncoupling protein, UCP1, which is responsible for the rapid generation of large amounts of heat at birth. Then, during postnatal life some, but not all, depots are replaced by white fat. This process can be utilised to investigate the physiological conversion of brown to white fat, and how it is re-programmed by nutritional changes in pre- and postnatal environments. A reduction in early BAT deposition may perpetuate through the life cycle, thereby suppressing energy expenditure and ultimately promoting obesity. Normal fat development profiles in the offspring are modified by changes in maternal diet at defined stages of pregnancy, ultimately leading to adverse long-term outcomes. For example, excess macrophage accumulation and the onset of insulin resistance occur in an adipose tissue depot-specific manner in offspring born to mothers fed a suboptimal diet from early to mid-gestation. In conclusion, the growth of the different fetal adipose tissue depots varies according to maternal diet and, if challenged in later life, this can contribute to insulin resistance and impaired glucose homeostasis.

摘要

脂肪组织的功能随发育而变化。在新生儿中,棕色脂肪组织(BAT)对于确保其有效适应宫外环境至关重要,其在妊娠期的生长在很大程度上依赖于母体向胎儿供应的葡萄糖。脂肪组织的沉积量、位置和类型也可以决定胎儿的葡萄糖稳态。脂肪组织大约在妊娠中期首次出现。总脂肪量随后在妊娠晚期增加,此时它由白色和棕色脂肪细胞的混合物组成。BAT 具有独特的解偶联蛋白 UCP1,它负责在出生时迅速产生大量热量。然后,在出生后的生命过程中,一些(但不是全部)脂肪库被白色脂肪所取代。这个过程可以用来研究棕色脂肪向白色脂肪的生理转化,以及它如何被产前和产后环境中营养变化重新编程。早期 BAT 沉积的减少可能会在整个生命周期中持续存在,从而抑制能量消耗,最终导致肥胖。在怀孕期间的特定阶段改变母体饮食会改变后代的正常脂肪发育模式,最终导致不良的长期后果。例如,在从妊娠早期到中期接受低质量饮食的母亲所生的后代中,脂肪组织沉积部位会出现巨噬细胞过度积累和胰岛素抵抗的发生。总之,不同胎儿脂肪组织沉积的生长根据母体饮食而变化,如果在以后的生活中受到挑战,这可能会导致胰岛素抵抗和葡萄糖稳态受损。

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Leptin, adiponectin and other adipokines in gestational diabetes mellitus and pre-eclampsia.妊娠糖尿病和子痫前期中的瘦素、脂联素和其他脂肪细胞因子。
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Inhibition of myostatin protects against diet-induced obesity by enhancing fatty acid oxidation and promoting a brown adipose phenotype in mice.
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Impact of prenatal exposure to delta 9-tetrahydrocannabinol and cannabidiol on birth size and postnatal growth trajectories.产前暴露于 Δ9-四氢大麻酚和大麻二酚对出生体重及产后生长轨迹的影响。
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