X1R3: how to indulge the gut's sweet tooth

摘要

While the increased GLP-1 secretion following stimulation with glucose was well established in vivo (6) and in vitro (21), the mechanisms underlying increased secretion were less clear. As an alternative approach to intestinal sweet taste receptors, the glucose-dependent closure of the K_(ATP) channel and the activation of sodium-glucose cotransporter (SGLT1) were considered important mediators of glucose-induced GLP-1 secretion, particularly due to the low expression levels of the taste transduction elements and a missing effect of artificial sweeteners in primary mouse L cells (22). Some other working groups also reported that artificial sweeteners do not stimulate GLP-1 secretion release in rodents and humans, questioning the role of the sweet taste receptor pathway in glucose-stimulated GLP-1 secretion (7, 15, 16). To address this controversy (for reviews see Refs. 20 and 24), further studies in mice lacking T1R2 and T1R3 were urgently needed to verify the role of the T1R2/T1R3 sweet taste receptor pathway in glucosestimulated GLP-1 secretion.