Greater Los Angeles Veteran Affairs Healthcare System, WLAVA Medical Center.
J Anim Sci. 2013 May;91(5):1957-62. doi: 10.2527/jas.2012-5941. Epub 2013 Jan 23.
Meal ingestion is followed by release of numerous hormones from enteroendocrine cells interspersed among the epithelial cells lining the intestine. Recently, the de-orphanization of G protein-coupled receptor (GPCR)-type nutrient receptors, expressed on the apical membranes of enteroendocrine cells, has suggested a plausible mechanism whereby luminal nutrients trigger the release of gut hormones. Activation of nutrient receptors triggers intracellular signaling mechanisms that promote exocytosis of hormone-containing granules into the submucosal space. Hormones released by foregut enteroendocrine cells include the glucagon-like peptides (GLP) affecting glycemic control (GLP-1) and releasing pro-proliferative, hypertrophy-inducing growth factors (GLP-2). The foregut mucosa, being exposed to pulses of concentrated HCl, is protected by a system of defense mechanisms, which includes epithelial bicarbonate and mucus secretion and augmentation of mucosal blood flow. We have reported that luminal co-perfusion of AA with nucleotides in anesthetized rats releases GLP-2 into the portal vein, associated with increased bicarbonate and mucus secretion and mucosal blood flow. The GLP-2 increases bicarbonate secretion via release of vasoactive intestinal peptide (VIP) from myenteric nerves. Luminal bile acids also release gut hormones due to activation of the bile-acid receptor known as G Protein-Coupled Receptor (GPR) 131, G Protein Bile Acid Receptor (GPBAR) 1, or Takeda G Protein-Coupled Receptor (TGR) 5, also expressed on enteroendocrine cells. The GLP are metabolized by dipeptidyl peptidase IV (DPPIV), an enzyme of particular interest to pharmaceutical, because its inhibition increases plasma concentrations of GLP-1 to treat diabetes. We have also reported that DPPIV inhibition enhances the secretory effects of nutrient-evoked GLP-2. Understanding the release mechanism and the metabolic pathways of gut hormones is of potential utility to the formulation of feedstuff additives that, by increasing nutrient absorption due to increased mucosal mass, can increase yields.
进食后,散布在肠道上皮细胞中的肠内分泌细胞会释放出许多激素。最近,G 蛋白偶联受体(GPCR)-型营养受体的去孤儿化,这些受体表达在肠内分泌细胞的顶膜上,提出了一种合理的机制,即腔内容物营养素触发肠激素的释放。营养受体的激活触发细胞内信号机制,促进含激素颗粒向黏膜下空间的胞吐作用。前肠内分泌细胞释放的激素包括影响血糖控制的胰高血糖素样肽(GLP)(GLP-1)和释放促增殖、促肥大诱导生长因子(GLP-2)。前肠黏膜暴露于浓缩盐酸脉冲中,受到防御机制的保护,包括上皮碳酸氢盐和黏液分泌以及黏膜血流增加。我们已经报道,在麻醉大鼠中,AA 与核苷酸的腔内共灌注会将 GLP-2 释放到门静脉中,同时伴有碳酸氢盐和黏液分泌以及黏膜血流增加。GLP-2 通过肠神经释放血管活性肠肽(VIP)来增加碳酸氢盐分泌。由于激活已知的胆汁酸受体 G 蛋白偶联受体(GPR)131、G 蛋白胆汁酸受体(GPBAR)1 或 Takeda G 蛋白偶联受体(TGR)5,腔内胆汁酸也会释放肠激素,这些受体也表达在肠内分泌细胞上。GLP 被二肽基肽酶 IV(DPPIV)代谢,这种酶对制药业特别感兴趣,因为其抑制会增加 GLP-1 的血浆浓度以治疗糖尿病。我们还报道,DPPIV 抑制增强了营养诱导的 GLP-2 的分泌作用。了解肠激素的释放机制和代谢途径对于制定饲料添加剂具有潜在的实用价值,这些添加剂可以通过增加黏膜质量来增加养分吸收,从而提高产量。