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母体高脂肪饮食通过胎儿脂肪组织的炎症变化引起胰岛素抵抗。

Maternal high-fat diets cause insulin resistance through inflammatory changes in fetal adipose tissue.

机构信息

Department of Obstetrics and Gynaecology, Mie University Graduate School of Medicine, Mie, Japan.

出版信息

Eur J Obstet Gynecol Reprod Biol. 2013 Jul;169(1):39-44. doi: 10.1016/j.ejogrb.2013.02.003. Epub 2013 Feb 27.

DOI:10.1016/j.ejogrb.2013.02.003
PMID:23453296
Abstract

OBJECTIVES

Epidemiological and animal studies have shown that maternal obesity predisposes the offspring to obesity and the metabolic syndrome, possibly via late-onset metabolic programming of the fetus. Little is known, however, about the metabolic effect of maternal obesity on the fetus. This study investigated the effect of a maternal high-fat diet (HFD) on fetal growth and glucose metabolism using a diet-induced obesity mouse model.

STUDY DESIGN

Female mice (6 weeks old; C57BL/6N) were fed either a normal chow diet (NCD, 10 kcal% fat) or an HFD (60 kcal% fat) for 4 weeks before mating and throughout pregnancy. At 17 days of gestation, gene expression of inflammatory markers and adipokines in fetal subcutaneous adipose tissue was analyzed by quantitative real-time polymerase chain reaction.

RESULTS

HFD mice were overweight, glucose intolerant and insulin resistant compared with NCD mice of the same gestational age. Although fetal body weight was not significantly different, fetal plasma glucose and insulin levels were higher in the HFD group than the NCD group. Furthermore, examination of fetal subcutaneous adipose tissue in the HFD group revealed hypertrophy with an increase in the levels of cluster of differentiation-68, chemokine receptor-2 and tumor necrosis factor-α mRNA, but a decrease in the level of glucose transporter-4 mRNA.

CONCLUSION

Maternal HFD causes inflammatory changes in the adipose tissue of offspring.

摘要

目的

流行病学和动物研究表明,母体肥胖使后代易患肥胖症和代谢综合征,这可能是通过胎儿晚期代谢编程实现的。然而,关于母体肥胖对胎儿代谢的影响知之甚少。本研究使用饮食诱导肥胖的小鼠模型,研究了母体高脂肪饮食(HFD)对胎儿生长和葡萄糖代谢的影响。

研究设计

雌性小鼠(6 周龄;C57BL/6N)在交配前和整个怀孕期间分别喂食正常饲料(NCD,10 kcal%脂肪)或 HFD(60 kcal%脂肪)4 周。在妊娠第 17 天,通过实时定量聚合酶链反应分析胎儿皮下脂肪组织中炎症标志物和脂肪因子的基因表达。

结果

与相同胎龄的 NCD 小鼠相比,HFD 小鼠超重、葡萄糖不耐受和胰岛素抵抗。尽管胎儿体重无显著差异,但 HFD 组的胎儿血浆葡萄糖和胰岛素水平高于 NCD 组。此外,在 HFD 组中检查胎儿皮下脂肪组织时发现,其存在肥大,CD68、趋化因子受体-2 和肿瘤坏死因子-α mRNA 水平升高,而葡萄糖转运蛋白-4 mRNA 水平降低。

结论

母体 HFD 导致后代脂肪组织发生炎症变化。

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