PDF(Pubmed)
Abstract：
Regulation of physiological homeostasis, including energy balance, is thought to be modified by low levels of adult neurogenesis in the hypothalamus. Hormones such as oestradiol can influence both embryonic and adult hypothalamic neurogenic programs, demonstrating a sensitivity of hypothalamic neural progenitor cells to endogenous hormones. Previously we showed that gestational exposure to environmental levels of the xenoestrogen bisphenol A (BPA) changed neural progenitor cell behaviors in the embryo; however, we did not examine if these changes were permanent to affect adult neurogenesis. Here we investigated whether adult neuro- and/or gliogenesis were altered in mice prenatally exposed to BPA and placed on a high-fat diet challenge. Gestationally exposed adult female mice on a standard diet gained less weight than non-BPA controls, whereas gestationally exposed BPA females on a high-fat diet gained more weight than controls. Males exposed to gestational BPA showed no differences in weight gain relative to control males. Concomitantly, adult neurogenesis was increased in the VMH, DMH, and PVN of adult female mice exposed to BPA on standard diet, suggesting that disrupted adult neurogenesis might perturb normal energy balance regulation in females. These results add to growing evidence that low-dose BPA exposure in utero causes changes to adult hypothalamic function.
摘要：
调节生理稳态，包括能量平衡，被认为是由下丘脑中低水平的成人神经发生改变的。激素如雌二醇可以影响胚胎和成人下丘脑神经原性程序，证明了下丘脑神经祖细胞对内源性激素的敏感性。以前我们发现，妊娠期暴露于环境水平的异种雌激素双酚A（BPA）改变了胚胎中的神经祖细胞行为；然而，我们没有检查这些变化是否永久影响成人神经发生.在这里，我们研究了在产前暴露于BPA并接受高脂肪饮食挑战的小鼠中，成年神经和/或胶质细胞生成是否发生了改变。接受标准饮食的成年雌性小鼠比非BPA对照组体重增加少，而妊娠期暴露于BPA的女性在高脂肪饮食中的体重增加超过对照组。暴露于妊娠BPA的男性相对于对照男性的体重增加没有差异。同时，在VMH中，成人神经发生增加，DMH,和在标准饮食下暴露于BPA的成年雌性小鼠的PVN，这表明成年神经发生中断可能会扰乱女性的正常能量平衡调节。这些结果增加了越来越多的证据，表明子宫内低剂量BPA暴露会导致成人下丘脑功能的变化。
