Maternal exposure to particulate matter derived from diesel exhaust has been shown to cause metabolic dysregulation, neurological problems, and increased susceptibility to diabetes in the offspring. Diesel exhaust is a major source of air pollution and the use of biodiesel (BD) and its blends have been progressively increasing throughout the world; however, studies on the health impact of BD vs. petrodiesel combustion-generated exhaust have been controversial in part, due to differences in the chemical and physical nature of the associated particulate matter (PM). To explore the long-term impact of prenatal exposure, pregnant mice were exposed to PM generated by combustion of petrodiesel (B0) and a 20% soy BD blend (B20) by intratracheal instillation during embryonic days 9–17 and allowed to deliver. Offspring were then followed for 52 weeks. We found that mother's exposure to B0 and B20 PM manifested in striking sex-specific phenotypes with respect to metabolic adaptation, maintenance of glucose homeostasis, and medial hypothalamic glial cell makeup in the offspring. The data suggest PM exposure limited to a narrower critical developmental window may be compensated for by the mother and/or the fetus by altered metabolic programming in a marked sex-specific and fuel-derived PM-specific manner, leading to sex-specific risk for diseases related to environmental exposure later in life.

母亲接触柴油机尾气中的颗粒物已被证明会导致后代代谢失调、神经系统问题和糖尿病易感性增加。柴油机尾气是空气污染的主要来源，生物柴油 （BD） 及其混合物的使用在全球范围内逐渐增加;然而，关于 BD 与汽油柴油燃烧产生的废气对健康影响的研究一直存在争议，部分原因是相关颗粒物 （PM） 的化学和物理性质存在差异。为了探讨产前暴露的长期影响，怀孕小鼠在胚胎第 9-17 天通过气管内滴注暴露于石油柴油 （B0） 和 20% 大豆 BD 混合物 （B20） 燃烧产生的 PM，并允许分娩。然后对后代进行 52 周的随访。我们发现，母亲暴露于 B0 和 B20 PM 表现为后代代谢适应、葡萄糖稳态维持和下丘脑内侧神经胶质细胞组成方面引人注目的性别特异性表型。数据表明，仅限于较窄的关键发育窗口的 PM 暴露可能由母亲和/或胎儿以显着的性别特异性和燃料衍生的 PM 特异性方式改变代谢程序来补偿，从而导致与环境暴露相关的疾病的性别特异性风险晚年。