Heptares Therapeutics Ltd BioPark, Broadwater Road, Welwyn Garden City, AL7 3AX, United Kingdom.
Pharmacol Res Perspect. 2015 Aug;3(4):e00155. doi: 10.1002/prp2.155. Epub 2015 Jul 7.
Gastrointestinal (GI) polypeptides are secreted from enteroendocrine cells (EECs). Recent technical advances and the identification of endogenous and synthetic ligands have enabled exploration of the pharmacology and physiology of EECs. Enteroendocrine signaling pathways stimulating hormone secretion involve multiple nutrient transporters and G protein-coupled receptors (GPCRs), which are activated simultaneously under prevailing nutrient conditions in the intestine following a meal. The majority of studies investigate hormone secretion from EECs in response to single ligands and although the mechanisms behind how individual signaling pathways generate a hormonal output have been well characterized, our understanding of how these signaling pathways converge to generate a single hormone secretory response is still in its infancy. However, a picture is beginning to emerge of how nutrients and full, partial, or allosteric GPCR ligands differentially regulate the enteroendocrine system and its interaction with the enteric and central nervous system. So far, activation of multiple pathways underlies drug discovery efforts to harness the therapeutic potential of the enteroendocrine system to mimic the phenotypic changes observed in patients who have undergone Roux-en-Y gastric surgery. Typically obese patients exhibit ∼30% weight loss and greater than 80% of obese diabetics show remission of diabetes. Targeting combinations of enteroendocrine signaling pathways that work synergistically may manifest with significant, differentiated EEC secretory efficacy. Furthermore, allosteric modulators with their increased selectivity, self-limiting activity, and structural novelty may translate into more promising enteroendocrine drugs. Together with the potential to bias enteroendocrine GPCR signaling and/or to activate multiple divergent signaling pathways highlights the considerable range of therapeutic possibilities available. Here, we review the pharmacology and physiology of the EEC system.
胃肠道(GI)多肽由肠内分泌细胞(EEC)分泌。最近的技术进步和内源性和合成配体的鉴定,使人们能够探索 EEC 的药理学和生理学。刺激激素分泌的肠内分泌信号通路涉及多种营养转运体和 G 蛋白偶联受体(GPCR),这些受体在餐后肠道中当前营养条件下同时被激活。大多数研究都在研究 EEC 对单个配体的激素分泌反应,尽管单个信号通路产生激素输出的机制已经得到很好的描述,但我们对这些信号通路如何汇聚以产生单一激素分泌反应的理解仍处于起步阶段。然而,目前已经开始了解营养物质和全、部分或变构 GPCR 配体如何差异调节肠内分泌系统及其与肠和中枢神经系统的相互作用。到目前为止,激活多种途径是药物发现努力的基础,旨在利用肠内分泌系统的治疗潜力来模拟接受 Roux-en-Y 胃手术的患者观察到的表型变化。通常肥胖患者的体重减轻约 30%,超过 80%的肥胖糖尿病患者的糖尿病得到缓解。靶向协同作用的肠内分泌信号通路组合可能具有显著的、差异化的 EEC 分泌效果。此外,具有增加的选择性、自限性活性和结构新颖性的变构调节剂可能转化为更有前途的肠内分泌药物。与偏向肠内分泌 GPCR 信号和/或激活多个发散信号通路的潜力相结合,突出了可用的治疗可能性的范围相当广泛。在这里,我们回顾了 EEC 系统的药理学和生理学。