Steensels Sandra, Vancleef Laurien, Depoortere Inge
Gut Peptide Lab, Translational Research Center for Gastrointestinal Disorders (TARGID), University of Leuven-KU Leuven, 3000 Leuven, Belgium.
Nutrients. 2016 Dec 7;8(12):795. doi: 10.3390/nu8120795.
Carbohydrate administration decreases plasma levels of the 'hunger hormone' ghrelin. The ghrelin cell is co-localized with the sweet taste receptor subunit, TAS1R3, and the gustatory G-protein, gustducin, both involved in the sensing of sweeteners by entero-endocrine cells. This study investigated the role of gustducin-mediated sweet taste receptor signaling on ghrelin secretion in a gastric ghrelinoma cell line, tissue segments and mice. The monosaccharide d-glucose and low-intensity sweetener oligofructose (OFS) decreased ( < 0.001) ghrelin secretion while the high-intensity sweetener sucralose increased ( < 0.001) ghrelin secretion in vitro. These effects were not mediated via the sweet taste receptor or glucose transporters (the sodium-dependent glucose cotransporter SGLT-1 and GLUT2). The effect of these compounds was mimicked ex vivo in gastric and jejunal segments from both wild type (WT) and α-gustducin knockout (α-gust) mice. In vivo, the sensing of d-glucose was polarized since intragastric but not intravenous administration of d-glucose decreased ( < 0.05) ghrelin levels in an α-gustducin independent manner which involved inhibition of duodenal ghrelin release. In contrast, neither OFS nor sucralose affected ghrelin secretion in vivo. In conclusion, α-gustducin-mediated sweet taste receptor signaling does not play a functional role in the sensing of carbohydrates, or low- or high-intensity sweeteners by the ghrelin cell.
碳水化合物的摄入会降低“饥饿激素”胃饥饿素的血浆水平。胃饥饿素细胞与甜味受体亚基TAS1R3和味觉G蛋白味导素共定位,这两者都参与肠内分泌细胞对甜味剂的感知。本研究调查了味导素介导的甜味受体信号传导在胃生长抑素瘤细胞系、组织切片和小鼠中对胃饥饿素分泌的作用。在体外,单糖d-葡萄糖和低强度甜味剂低聚果糖(OFS)可降低(<0.001)胃饥饿素的分泌,而高强度甜味剂三氯蔗糖则可增加(<0.001)胃饥饿素的分泌。这些作用并非通过甜味受体或葡萄糖转运蛋白(钠依赖性葡萄糖共转运蛋白SGLT-1和GLUT2)介导。在野生型(WT)和α-味导素基因敲除(α-gust)小鼠的胃和空肠段中,这些化合物的作用在体外得到了模拟。在体内,d-葡萄糖的感知是极化的,因为胃内而非静脉注射d-葡萄糖以α-味导素非依赖性方式降低(<0.05)胃饥饿素水平,这涉及抑制十二指肠胃饥饿素的释放。相比之下,OFS和三氯蔗糖在体内均不影响胃饥饿素的分泌。总之,α-味导素介导的甜味受体信号传导在胃饥饿素细胞对碳水化合物或低强度或高强度甜味剂的感知中不起作用。