Ventromedial hypothalamic lesion-induced vagal hyperactivity stimulates rat pancreatic cell proliferation
Ventromedial hypothalamic lesion-induced vagal hyperactivity stimulates rat pancreatic cell proliferation
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DOI：
10.1053/gast.1996.v110.pm8608899
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发表时间：
1996-03-01
期刊：
影响因子：
29.4
通讯作者：
Inoue, S
中科院分区：
文献类型：
--
作者：
Kiba, T;Tanaka, K;Inoue, S
背景与目的：大鼠下丘脑腹内侧核（VMH）损伤可引起胰腺DNA含量增加。本研究探讨了VMH损伤形成后，细胞增殖在大鼠胰腺有丝分裂反应中的作用。研究方法：在VMH损伤形成后0、1、3和7天，测量大鼠胰腺DNA含量、DNA合成和抗增殖细胞核抗原分子抗体标记指数的变化。此外，研究迷走神经切断术、阿托品或抗胰岛素抗体对VMH损伤诱导的DNA合成改变的影响。胰腺样本也进行了双重免疫染色：首先为PCNA，然后为胰岛素，胰高血糖素，生长抑素。结果：VMH损伤组胰腺重量、DNA含量和DNA合成增加。VMH损伤形成后1天开始，主要在胰岛B和腺泡细胞中观察到增殖，3天后达到最大速率。VMH损伤诱导的DNA合成的刺激被完全抑制迷走神经切断术或阿托品管理，但不是由抗胰岛素抗体。结论：VMH损伤引起的迷走神经亢进主要通过胆碱能受体机制刺激大鼠胰岛B和腺泡细胞增殖。
Background & Aims: Ventromedial hypothalamic (VMH) lesions cause an increase in DNA content in the rat pancreas. This study examined the role of cell proliferation in the mitotic response of the rat pancreas after VMH lesion formation. Methods: Alterations in rat pancreatic DNA content, DNA synthesis, and labeling indices using antiproliferation cell nuclear antigen molecular antibody were measured 0, 1, 3, and 7 days after VMH lesion formation. Additionally, the effects of vagotomy, atropine, or anti-insulin antibody on VMH lesion-induced alterations in DNA synthesis were examined. Pancreatic samples were also treated with double immunostaining: first for PCNA and then for insulin, glucagon, and somatostatin. Results: Pancreatic weight, DNA content, and DNA synthesis increased in animals receiving VMH lesions. Proliferation was primarily observed in islet B and acinar cells beginning 1 day after VMH lesion formation, reaching a maximum rate after 3 days. VMH lesion-induced stimulation of DNA synthesis was completely inhibited by vagotomy or atropine administration but not by anti-insulin antibody. Conclusions: Vagal hyperactivity produced by VMH lesions stimulates cell proliferation of rat pancreatic islet B and acinar cells primarily through a cholinergic receptor mechanism.