Abstract
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 (p < 0.001) ghrelin secretion while the high-intensity sweetener sucralose increased (p < 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 (p < 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.
Highlights
Over the past four decades, we have transitioned from a world in which underweight prevalence was more than double that of obesity, to one in which more people are obese than underweight [1].This increase in obesity prevalence has been linked to an excessive sugar intake [2,3]
This study aimed to investigate whether α-gustducin mediated sweet taste receptor signaling is involved in the effect of carbohydrates and sweeteners on ghrelin release
The gastric MGN3-1 cell line shows a strong expression of the TAS1R3 subunit of the sweet taste receptor and the glucose transporters (SGLT1 and GLUT2)
Summary
Over the past four decades, we have transitioned from a world in which underweight prevalence was more than double that of obesity, to one in which more people are obese than underweight [1].This increase in obesity prevalence has been linked to an excessive sugar intake [2,3]. Guidelines in healthcare arose, recommending reductions in added sugar intake [4] Sugar replacers, such as high-intensity sweeteners (HIS, e.g., sucralose), can help reduce the sugar content of meals without affecting its taste. These sweeteners are non-caloric but might not be metabolically inert, since contradictory results have been reported on their impact on energy homeostasis [5]. OFS has a low caloric content (1.7 kcal/g) which is derived from its microbial fermentation products, the short-chain fatty acids (SCFAs), which can be used as an energy substrate by the colonocytes It has a sweetening power of 35% of that of sucrose (table sugar) [6]
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