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Xenin delays gastric emptying rate and activates the brainstem in mice.

机译:Xenin可延缓小鼠的胃排空速度并激活脑干。

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摘要

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.
机译:Xenin是一种25个氨基酸的胃肠道肽,通过作用于中枢神经系统来抑制进食。胃肠激素可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,Xenin通过脑干细胞的活化来延迟胃排空。为了解决这个假设,我们检查了腹膜内(i.p.)注射Xenin对小鼠胃排空率和脑干Fos表达的影响。与用盐水处理的对照小鼠相比,用氙气处理的小鼠的胃排空率降低了约93%。 i.p. Xenin注射显着增加了脑干孤立道(NTS)核中的Fos免疫反应细胞,但没有增加区域后部区域(AP)和迷走神经背运动核(DMV)。这些发现支持了这样的假说,即Xenin引起的厌食症至少部分是由于胃排空延迟和NTS细胞活化引起的。

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