Kentish Stephen J, Li Hui, Frisby Claudine L, Page Amanda J
Vagal Afferent Research Group, Centre for Nutrition and Gastrointestinal Disease, Discipline of Medicine, University of Adelaide, Frome Road, Adelaide, SA 5005, Australia; Nutrition and Metabolism, South Australian Health and Medical Research Institute, North Terrace, SA 5000, Australia; School of Medicine, University of Queensland, St Lucia, QLD 4067, Australia.
Vagal Afferent Research Group, Centre for Nutrition and Gastrointestinal Disease, Discipline of Medicine, University of Adelaide, Frome Road, Adelaide, SA 5005, Australia; Nutrition and Metabolism, South Australian Health and Medical Research Institute, North Terrace, SA 5000, Australia.
Peptides. 2017 Mar;89:35-41. doi: 10.1016/j.peptides.2017.01.005. Epub 2017 Jan 10.
Food intake is regulated by vagal afferent signals from the stomach. Nesfatin-1 is an anorexigenic peptide produced within the gastrointestinal tract and has well defined central effects. We aimed to determine if nesfatin-1 can modulate gastric vagal afferent signals in the periphery and further whether this is altered in different nutritional states. Female C57BL/6J mice were fed either a standard laboratory diet (SLD) or a high fat diet (HFD) for 12 weeks or fasted overnight. Plasma nucleobindin-2 (NUCB2; nesfatin-1 precursor)/nesfatin-1 levels were assayed, the expression of NUCB2 in the gastric mucosa and adipose tissue was assessed using real-time quantitative reverse-transcription polymerase chain reaction. An in vitro preparation was used to determine the effect of nesfatin-1 on gastric vagal afferent mechanosensitivity. HFD mice exhibited an increased body weight and adiposity. Plasma NUCB2/nesfatin-1 levels were unchanged between any of the groups of mice. NUCB2 mRNA was detected in the gastric mucosa and gonadal fat of SLD, HFD and fasted mice with no difference in mRNA abundance between groups in either tissue. In SLD and fasted mice nesfatin-1 potentiated mucosal receptor mechanosensitivity, an effect not observed in HFD mice. Tension receptor mechanosensitivity was unaffected by nesfatin-1 in SLD and fasted mice, but was inhibited in HFD mice. In conclusion, Nesfatin-1 modulates gastric vagal afferent mechanosensitivity in a nutritional state dependent manner.
食物摄入量受来自胃部的迷走神经传入信号调节。Nesfatin-1是一种在胃肠道内产生的厌食肽，具有明确的中枢作用。我们旨在确定Nesfatin-1是否能在外周调节胃迷走神经传入信号，以及在不同营养状态下这种调节是否会发生改变。将雌性C57BL/6J小鼠分别喂食标准实验室饮食（SLD）或高脂饮食（HFD）12周，或禁食过夜。检测血浆核结合蛋白-2（NUCB2；Nesfatin-1前体）/Nesfatin-1水平，使用实时定量逆转录聚合酶链反应评估胃黏膜和脂肪组织中NUCB2的表达。采用体外实验制剂来确定Nesfatin-1对胃迷走神经传入机械敏感性的影响。HFD小鼠体重和肥胖程度增加。各组小鼠之间血浆NUCB2/Nesfatin-1水平无变化。在SLD、HFD和禁食小鼠的胃黏膜和性腺脂肪中均检测到NUCB2 mRNA，两组小鼠在任一组织中的mRNA丰度均无差异。在SLD和禁食小鼠中，Nesfatin-1增强了黏膜受体机械敏感性，而在HFD小鼠中未观察到这种效应。在SLD和禁食小鼠中，张力受体机械敏感性不受Nesfatin-1影响，但在HFD小鼠中受到抑制。总之，Nesfatin-1以营养状态依赖的方式调节胃迷走神经传入机械敏感性。
