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迷走神经和腹腔肠系膜神经节参与雄性 Sprague Dawley 大鼠非硫酸化胆囊收缩素-8 诱导的进食反应。

The Vagus Nerve and the Celiaco-mesenteric Ganglia Participate in the Feeding Responses Evoked by Non-sulfated Cholecystokinin-8 in Male Sprague Dawley Rats.

机构信息

Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, AL, USA.

Department of Anatomy and Histology, College of Veterinary Medicine, Basra University, Basra, Iraq.

出版信息

Endocr Res. 2020 Feb-May;45(2):73-83. doi: 10.1080/07435800.2019.1670673. Epub 2019 Oct 1.

Abstract

We have shown that non-sulfated cholecystokinin-8 (NS CCK-8) reduces food intake in adult male Sprague Dawley rats by activating cholecystokinin-B receptor (CCK-BR). Here, we tested the hypothesis that the vagus nerve and the celiaco-mesenteric ganglia may play a role in this reduction. The hypothesis stems from the following facts. The vagus and the celiaco-mesenteric ganglia contain NS CCK-8, they express and have binding sites for CCK-BR, NS CCK-8 activates CCK-BR on afferent vagal and sympathetic fibers and the two structures link the gastrointestinal tract to central feeding nuclei in the brain, which also contain the peptide and CCK-BR. To test this hypothesis, three groups of free-feeding rats, vagotomy (VGX), celiaco-mesenteric ganglionectomy (CMGX) and sham-operated, received NS CCK-8 (0, 0.5 and 1 nmol/kg) intraperitoneally prior to the onset of the dark cycle and various feeding behaviors were recorded. We found that in sham-operated rats both doses of NS CCK-8 reduced meal size (MS), prolonged the intermeal interval (IMI, time between first and second meal), increased satiety ratio (SR = IMI/MS), reduced 24-h food intake and reduced the number of meals relative to saline control. In the VGX and the CMGX groups, all of the previous responses were attenuated. Consistent with our hypothesis, the findings of the current work suggest a role for the vagus nerve and the celiaco-mesenteric ganglia in the feeding responses evoked by NS CCK-8.

摘要

我们已经证明,非硫酸化胆囊收缩素-8(NS CCK-8)通过激活胆囊收缩素-B 受体(CCK-BR)来减少成年雄性 Sprague Dawley 大鼠的食物摄入。在这里,我们测试了这样一个假设,即迷走神经和腹腔肠系膜神经节可能在这种减少中发挥作用。这一假设源于以下事实。迷走神经和腹腔肠系膜神经节含有 NS CCK-8,它们表达并具有 CCK-BR 的结合位点,NS CCK-8 激活传入迷走神经和交感神经纤维上的 CCK-BR,这两个结构将胃肠道与大脑中的中枢摄食核连接起来,而大脑中的中枢摄食核也含有肽和 CCK-BR。为了验证这一假设,三组自由进食的大鼠(迷走神经切断术(VGX)、腹腔肠系膜神经节切除术(CMGX)和假手术)在暗周期开始前接受腹腔内注射 NS CCK-8(0、0.5 和 1 nmol/kg),并记录各种进食行为。我们发现,在假手术组中,两种剂量的 NS CCK-8 均减少了餐量(MS),延长了进食间隔(IMI,第一次和第二次进食之间的时间),增加了饱食比(SR = IMI/MS),减少了 24 小时的食物摄入量,并减少了相对于盐水对照的进食次数。在 VGX 和 CMGX 组中,所有上述反应均减弱。与我们的假设一致,当前工作的发现表明,迷走神经和腹腔肠系膜神经节在 NS CCK-8 引起的进食反应中起作用。

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