SummaryMaternal obesity is a well‐known risk factor for developing premature obesity, metabolic syndrome, cardiovascular disease and type 2 diabetes in the progeny. The development of white adipose tissue is a dynamic process that starts during prenatal life: fat depots laid down in utero are associated with the proportion of fat in children later on. How early this programming takes place is still unknown. However, recent evidence shows that mesenchymal stem cells (MSC), the embryonic adipocyte precursor cells, show signatures of the early setting of an adipogenic committed phenotype when exposed to maternal obesity. This review aims to present current findings on the cellular adaptations of MSCs from the offspring of women with obesity and how the metabolic environment of MSCs could affect the early commitment towards adipocytes. In conclusion, maternal obesity can induce early programming of fetal adipose tissue by conditioning MSCs. These cells have higher expression of adipogenic markers, altered insulin signalling and mitochondrial performance, compared to MSCs of neonates from lean pregnancies. Fetal MSCs imprinting by maternal obesity could help explain the increased risk of childhood obesity and development of further noncommunicable diseases.

中文翻译：

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间充质干细胞在肥胖女性后代脂肪组织早期编程中的作用

概括众所周知，母亲肥胖是导致后代出现过早肥胖、代谢综合征、心血管疾病和 2 型糖尿病的危险因素。白色脂肪组织的发育是一个从产前开始的动态过程：子宫内沉积的脂肪库与以后儿童的脂肪比例相关。这种编程发生的时间有多早仍然未知。然而，最近的证据表明，间充质干细胞（MSC），即胚胎脂肪细胞前体细胞，在母亲肥胖的情况下显示出早期形成脂肪形成定型表型的特征。本综述旨在介绍肥胖女性后代间充质干细胞细胞适应性的最新发现，以及间充质干细胞的代谢环境如何影响脂肪细胞的早期分化。总之，母亲肥胖可以通过调节 MSC 来诱导胎儿脂肪组织的早期编程。与瘦妊娠新生儿的 MSC 相比，这些细胞具有更高的脂肪生成标志物表达、胰岛素信号传导和线粒体性能改变。母亲肥胖造成的胎儿间充质干细胞印记可能有助于解释儿童肥胖风险增加和进一步发展非传染性疾病的风险。