Department of Physiology, University of Manitoba, Winnipeg, MB R3E0J9, Canada.
Neurosci Lett. 2010 Aug 30;481(1):59-63. doi: 10.1016/j.neulet.2010.06.055. Epub 2010 Jun 25.
Xenin, a 25-amino acid gastrointestinal peptide, inhibits feeding by acting through the central nervous system. Gastrointestinal hormones reduce food intake partly by activating the brainstem and inhibiting gastric emptying. Therefore, we hypothesized that xenin delays gastric emptying through the activation of the brainstem cells. To address this hypothesis, we examined the effect of intraperitoneal (i.p.) injection of xenin on gastric emptying rate and brainstem Fos expression in mice. Gastric emptying rate was reduced by about 93% in xenin-treated mice compared to saline-treated control mice. The i.p. xenin injection significantly increased Fos-immunoreactive cells in the nucleus of the solitary tract (NTS) of the brainstem, but not area postrema (AP) and dorsal motor nucleus of the vagus (DMV). These findings support the hypothesis that xenin-induced anorexia is at least partly due to delayed gastric emptying and the activation of the NTS cells.
食欲素是一种 25 个氨基酸的胃肠道肽,通过中枢神经系统发挥抑制进食作用。胃肠激素通过激活脑干和抑制胃排空来部分减少食物摄入。因此,我们假设食欲素通过激活脑干细胞来延迟胃排空。为了验证这一假设,我们研究了腹腔内(i.p.)注射食欲素对小鼠胃排空率和脑干 Fos 表达的影响。与生理盐水处理的对照组小鼠相比,食欲素处理的小鼠胃排空率降低了约 93%。腹腔注射食欲素显著增加了脑干孤束核(NTS)中 Fos-免疫反应细胞,但不增加极后区(AP)和迷走神经背核(DMV)中的 Fos-免疫反应细胞。这些发现支持了这样的假设,即食欲素诱导的厌食至少部分是由于胃排空延迟和 NTS 细胞的激活。