CURE/Digestive Diseases Research Center, and Center for Neurobiology of Stress, Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles and VA Greater Los Angeles Healthcare System, Los Angeles, California, USA.
Am J Physiol Gastrointest Liver Physiol. 2010 Jan;298(1):G45-56. doi: 10.1152/ajpgi.00349.2009. Epub 2009 Nov 5.
Peptide YY (PYY) antisecretory effect on intestinal epithelia is well established, whereas less is known about its actions to influence colonic motility in conscious animals. We characterized changes in basal function and stimulated colonic motor function induced by PYY-related peptides in conscious mice. PYY(3-36), PYY, and neuropeptide Y (NPY) (8 nmol/kg) injected intraperitoneally inhibited fecal pellet output (FPO) per hour during novel environment stress by 90%, 63%, and 57%, respectively, whereas the Y(1)-preferring agonists, [Pro(34)]PYY and [Leu(31),Pro(34)]NPY, had no effect. Corticotrophin-releasing factor 2 receptor antagonist did not alter PYY(3-36) inhibitory action. PYY and PYY(3-36) significantly reduced restraint-stimulated defecation, and PYY(3-36) inhibited high-amplitude distal colonic contractions in restrained conscious mice for 1 h, by intraluminal pressure with the use of a microtransducer. PYY suppression of intraperitoneal 5-hydroxytryptophan induced FPO and diarrhea was blocked by the Y(2) antagonist, BIIE0246, injected intraperitoneally and mimicked by PYY(3-36), but not [Leu(31),Pro(34)]NPY. PYY(3-36) also inhibited bethanechol-stimulated FPO and diarrhea. PYY(3-36) inhibited basal FPO during nocturnal feeding period and light phase in fasted/refed mice for 2-3 h, whereas the reduction of food intake lasted for only 1 h. PYY(3-36) delayed gastric emptying after fasting-refeeding by 48% and distal colonic transit time by 104%, whereas [Leu(31),Pro(34)]NPY had no effect. In the proximal and distal colon, higher Y(2) mRNA expression was detected in the mucosa than in muscle layers, and Y(2) immunoreactivity was located in nerve terminals around myenteric neurons. These data established that PYY/PYY(3-36) potently inhibits basal and stress/serotonin/cholinergic-stimulated propulsive colonic motor function in conscious mice, likely via Y(2) receptors.
肽 YY(PYY)对肠道上皮的抗分泌作用已得到充分证实,而其影响清醒动物结肠运动的作用知之甚少。我们描述了 PYY 相关肽在清醒小鼠中对基础功能和刺激结肠运动功能的影响。腹腔内注射 PYY(3-36)、PYY 和神经肽 Y(NPY)(8 nmol/kg)分别抑制了新环境应激下每小时粪便颗粒排出量(FPO)的 90%、63%和 57%,而 Y1- 偏好激动剂[Pro34]PYY 和[Leu31,Pro34]NPY 则没有作用。皮质激素释放因子 2 受体拮抗剂不能改变 PYY(3-36)的抑制作用。PYY 和 PYY(3-36)显著减少束缚刺激的排便,并且 PYY(3-36)通过微传感器在腔内压力下抑制束缚清醒小鼠 1 小时内的高振幅远端结肠收缩。腹腔内 5-羟色氨酸诱导的 FPO 和腹泻被腹腔内注射的 Y2 拮抗剂 BIIE0246 阻断,并被 PYY(3-36)模拟,但[Leu31,Pro34]NPY 则没有。PYY(3-36)还抑制了 Bethanechol 刺激的 FPO 和腹泻。PYY(3-36)在禁食/再喂养的夜间进食期间和快速/再喂养的小鼠的光相期间抑制基础 FPO2-3 小时,而食物摄入量的减少仅持续 1 小时。PYY(3-36)使禁食/再喂养后的胃排空延迟 48%,远端结肠通过时间延迟 104%,而[Leu31,Pro34]NPY 则没有作用。在近端和远端结肠中,在黏膜中检测到更高的 Y2 mRNA 表达,而在肌肉层中则较低,并且 Y2 免疫反应性位于肌间神经元周围的神经末梢中。这些数据表明,PYY/PYY(3-36)在清醒小鼠中强烈抑制基础和应激/5-羟色胺/胆碱能刺激的推进性结肠运动功能,可能通过 Y2 受体。