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Maternal food restriction‐induced intrauterine growth restriction in a rat model leads to sex‐specific adipogenic programming
The FASEB Journal ( IF 4.4 ) Pub Date : 2020-10-13 , DOI: 10.1096/fj.202000985rr
Sreevidya Sreekantha 1, 2 , Ying Wang 1, 2 , Reiko Sakurai 1, 2 , Jie Liu 1, 2 , Virender K Rehan 1, 2
Affiliation  

Intrauterine growth restriction (IUGR) leads to offspring obesity. In a maternal food restriction (MFR) during pregnancy‐related IUGR rat model, bone marrow stem cells showed enhanced adipogenic programming; however, the effect of IUGR on white adipose tissue (WAT) progenitors is unknown. Here, by mRNA and functional profiling, we determined sex‐specific adipogenic programming of WAT progenitors isolated from pups on the postnatal day (PND) 1 and 21. On PND1, PPARγ and Pref‐1 expression was significantly downregulated in preadipocytes of both MFR males and females; however, at PND21, preadipocytes of MFR males showed upregulation in these genes. Even following adipogenic induction, both male and female MFR adipocytes exhibited lower PPARγ, ADRP, and adiponectin levels at PND1; however, at PND21 MFR male adipocytes showed an upward trend in the expression of these genes. An adipogenesis‐specific RT‐PCR array showed that male MFR adipocytes were programmed to exhibit stronger adipogenic propensity than females. Last, serum sex hormone and adipocyte estrogen/testosterone receptor expression profiles provide preliminary insights into the possible mechanism underlying sex‐specific adipogenic programming in the IUGR offspring. In summary, IUGR programs WAT preadipocytes to greater adipogenic potential in males. Although the altered adipogenic programming following MFR was detectable at PND1, the changes were more pronounced at PND21, suggesting a potential role of postnatal nutrition in facilitating the sex‐specific adipogenic programming in the IUGR offspring.

中文翻译:


在大鼠模型中,母体食物限制诱导的宫内生长限制导致性别特异性脂肪形成编程



宫内生长受限(IUGR)会导致后代肥胖。在妊娠期间母亲食物限制(MFR)相关的 IUGR 大鼠模型中,骨髓干细胞显示出增强的脂肪生成编程;然而,IUGR 对白色脂肪组织 (WAT) 祖细胞的影响尚不清楚。在这里,通过 mRNA 和功能分析,我们确定了出生后第 1 天和第 21 天从幼崽中分离出的 WAT 祖细胞的性别特异性脂肪形成编程。在 PND1 上,两种 MFR 雄性的前脂肪细胞中 PPARγ 和 Pref-1 表达显着下调和女性;然而,在 PND21 时,MFR 男性的前脂肪细胞显示这些基因上调。即使在脂肪形成诱导后,雄性和雌性 MFR 脂肪细胞在 PND1 时都表现出较低的 PPARγ、ADRP 和脂联素水平。然而,在 PND21 MFR 时,雄性脂肪细胞这些基因的表达呈上升趋势。脂肪生成特异性 RT-PCR 阵列显示,男性 MFR 脂肪细胞被编程为表现出比女性更强的脂肪生成倾向。最后,血清性激素和脂肪细胞雌激素/睾酮受体表达谱为 IUGR 后代性别特异性脂肪形成编程的可能机制提供了初步见解。总之,IUGR 对 WAT 前脂肪细胞进行编程,以提高男性的成脂潜力。尽管在 PND1 时可检测到 MFR 后脂肪生成程序的改变,但在 PND21 时变化更为明显,这表明产后营养在促进 IUGR 后代的性别特异性脂肪生成程序中具有潜在作用。
更新日期:2020-10-13
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