Gestational diabetes mellitus (GDM) has been strongly associated with an increased risk of type 2 diabetes mellitus (T2DM) in later child and adulthood. The human umbilical cord and its contents are of fetal origin and represent the fetus genetically and physiologically. Since it is not possible to obtain tissues from the fetus and newborn to investigate the association between GDM and later T2DM, we reprogrammed the stem cells from the Wharton’s jelly of umbilical cords (hWJSCs) of GDM and non-GDM mothers into induced pluripotent stem cells (iPSCs) and then differentiated the iPSCs into insulin-producing cells (IPCs) to provide pancreatic tissues that represent the fetus of GDM and normal mothers. These tissues are an attractive model to study the effects of glucose on the fetus. Interestingly, GDM-iPSCs had a decreased potential towards differentiation into IPCs. IPCs differentiated from GDM-iPSCs also had lower total insulin content and a lower capacity for insulin secretion to glucose stimulation compared to their normal-iPSC counterparts. This abnormal pathogenesis in GDM-iPSCs pancreatic differentiation recapitulates the pathology that may be observed in the infants of the diabetic mother (IDM) and while indicating adaptive mechanisms for fetal survival, may lead to the development of T2DM later in life. (199 words)

妊娠糖尿病（GDM）与后期儿童和成年后2型糖尿病（T2DM）风险增加密切相关。人的脐带及其内容物是胎儿来源的，从遗传和生理上代表胎儿。由于不可能从胎儿和新生儿获得组织来研究GDM和后来的T2DM之间的关联，因此我们将来自GDM和非GDM母亲的沃顿氏脐带（hWJSCs）的干细胞重新编程为诱导性多能干细胞（iPSC），然后将其分化为产生胰岛素的细胞（IPC），以提供代表GDM胎儿和正常母亲的胰腺组织。这些组织是研究葡萄糖对胎儿影响的诱人模型。有趣的是 GDM-iPSC分化为IPC的潜力降低。与普通iPSC对应物相比，与GDM-iPSC区别开来的IPC还具有较低的总胰岛素含量和较低的胰岛素分泌能力。GDM-iPSCs胰腺分化的这种异常发病机理概括了在糖尿病母亲（IDM）的婴儿中可能观察到的病理，虽然表明胎儿存活的适应机制，但可能导致T2DM在以后的生活中发展。（199个字）GDM-iPSCs胰腺分化的这种异常发病机理概括了在糖尿病母亲（IDM）的婴儿中可能观察到的病理，虽然表明胎儿存活的适应机制，但可能导致T2DM在以后的生活中发展。（199个字）GDM-iPSCs胰腺分化的这种异常发病机理概括了在糖尿病母亲（IDM）的婴儿中可能观察到的病理，虽然表明胎儿存活的适应性机制可能会导致T2DM在以后的生活中发展。（199个字）