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孕期营养增加可刺激出生前脂肪组织中过氧化物酶体增殖物激活受体γ、脂联素和瘦素信使核糖核酸的表达。

Increased maternal nutrition stimulates peroxisome proliferator activated receptor-gamma, adiponectin, and leptin messenger ribonucleic acid expression in adipose tissue before birth.

作者信息

Muhlhausler B S, Duffield J A, McMillen I C

机构信息

Sansom Research Institute, University of South Australia, Adelaide 5000, South Australia, Australia.

出版信息

Endocrinology. 2007 Feb;148(2):878-85. doi: 10.1210/en.2006-1115. Epub 2006 Oct 26.

DOI:10.1210/en.2006-1115
PMID:17068138
Abstract

During fetal life, adipose tissue is predominantly comprised of brown or thermogenic adipocytes and there is a transition to white, lipid-storing adipocytes after birth concomitant with the onset of suckling. In pregnancies complicated by gestational diabetes, the fetus is hyperglycemic, has an increased fat mass, and is at increased risk of obesity in later life. In the present study, we have investigated the hypothesis that exposure to increased maternal nutrition during late gestation results in increased expression of genes that regulate adipogenesis and lipogenesis in perirenal fat in fetal sheep. Pregnant ewes were fed either at or approximately 55% above maintenance energy requirements during late pregnancy and quantitative RT-PCR was used to measure peroxisome proliferator-activated receptor gamma, lipoprotein lipase, glycerol-3-phosphate dehydrogenase, adiponectin, and leptin mRNA expression. We report that exposure to metabolic and hormonal signals of increased nutrition before birth results in an increase in the expression of the adipogenic factor, peroxisome proliferator-activated receptor gamma, and in lipoprotein lipase, adiponectin, and leptin mRNA expression in fetal perirenal fat. We propose that an increase in maternal, and hence fetal, nutrition results in a precocial increase in adipogenic, lipogenic, and adipokine gene expression in adipose tissue and that these changes may be important in the development of obesity in later life.

摘要

在胎儿期,脂肪组织主要由棕色或产热脂肪细胞组成,出生后随着哺乳开始,会向储存脂质的白色脂肪细胞转变。在患有妊娠期糖尿病的妊娠中,胎儿血糖过高,脂肪量增加,且成年后肥胖风险增加。在本研究中,我们探讨了以下假说:妊娠晚期母体营养增加会导致胎羊肾周脂肪中调节脂肪生成和脂质生成的基因表达增加。在妊娠晚期,给怀孕母羊喂食维持能量需求水平或比维持能量需求高约55%的饲料,并使用定量RT-PCR来测量过氧化物酶体增殖物激活受体γ、脂蛋白脂肪酶、甘油-3-磷酸脱氢酶、脂联素和瘦素的mRNA表达。我们报告称,出生前暴露于营养增加的代谢和激素信号会导致脂肪生成因子过氧化物酶体增殖物激活受体γ以及胎儿肾周脂肪中脂蛋白脂肪酶、脂联素和瘦素mRNA表达增加。我们认为,母体营养增加进而胎儿营养增加会导致脂肪组织中脂肪生成、脂质生成和脂肪因子基因表达过早增加,且这些变化可能对成年后肥胖的发展具有重要意义。

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