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由缺乏缬氨酸的饮食引起的大鼠厌食症不能通过全身给予胃饥饿素治疗得到改善。

Anorexia in rats caused by a valine-deficient diet is not ameliorated by systemic ghrelin treatment.

机构信息

Department of Veterinary Physiology, Miyazaki University, Miyazaki, Miyazaki 889-2192, Japan.

出版信息

Neuroscience. 2010 Mar 10;166(1):333-40. doi: 10.1016/j.neuroscience.2009.12.013. Epub 2009 Dec 17.

Abstract

Rodents exhibit aversive behavior toward a diet that lacks at least one of the essential amino acids. We sought to determine whether the particular form of anorexia caused by such diets could be ameliorated by the administration of orexigenic peptides while simultaneously analyzing the neural mechanisms underlying anorexia. Rats were fed a valine-deficient diet, which induced severe anorexia (reducing food consumption by 80%). The severe anorexia was associated with a significant decrease in the cerebrospinal fluid valine concentration and hyper-ghrelinemia. Between 6 and 12 days after initiation of the valine-deficient diet, we injected rats twice daily with valine and/or an orexigenic peptide (ghrelin, neuropeptide Y, or agouti-related protein) either i.p. or i.c.v.. We then measured dietary intake. An i.c.v. valine injection allowed earlier food intake compared with an i.p valine injection and increased the density of c-Fos-positive ependymal cells lining the third ventricle. Whereas an i.c.v. injection of ghrelin or neuropeptide Y increased consumption of the valine-deficient diet, i.p injection of ghrelin or i.c.v. injection of agouti-related protein did not. Following i.c.v. administration of either valine or ghrelin, we did not observe complete recovery of consumption of the valine-deficient diet. This may be due to the ineffectiveness of peripheral ghrelin and central agouti-related protein and/or to conditioned aversion to the valine-deficient diet. Since ghrelin is known to be involved in food anticipatory activities, whether the hyper-ghrelinemia observed in valine-deficient rats play role in foraging behavior other than food intake is the future study to be investigated.

摘要

啮齿动物表现出对缺乏至少一种必需氨基酸的饮食的厌恶行为。我们试图确定,当同时分析厌食症的神经机制时,这种饮食引起的特殊形式的厌食症是否可以通过给予食欲肽来改善。老鼠喂食缺乏缬氨酸的饮食,这会导致严重的厌食症(减少 80%的食物摄入量)。严重的厌食症与脑脊液缬氨酸浓度显着降低和高胃饥饿素血症有关。在开始缺乏缬氨酸的饮食后 6 至 12 天,我们每天两次通过 i.p 或 i.c.v 给老鼠注射缬氨酸和/或食欲肽(胃饥饿素,神经肽 Y 或 agouti 相关蛋白)。然后测量饮食摄入量。与 i.p 缬氨酸注射相比,脑室注射缬氨酸可更早地摄入食物,并增加第三脑室衬里的 c-Fos 阳性室管膜细胞的密度。尽管脑室注射胃饥饿素或神经肽 Y 增加了对缺乏缬氨酸的饮食的消耗,但 i.p 注射胃饥饿素或 i.c.v 注射 agouti 相关蛋白则没有。在 i.c.v 给予缬氨酸或胃饥饿素后,我们没有观察到对缺乏缬氨酸的饮食的消耗完全恢复。这可能是由于外周胃饥饿素和中枢 agouti 相关蛋白无效,和/或对缺乏缬氨酸的饮食产生条件性厌恶。由于已知胃饥饿素参与食物预期活动,因此观察到缺乏缬氨酸的大鼠中高胃饥饿素血症是否在除食物摄入之外的觅食行为中发挥作用,是未来需要研究的课题。

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