Sensing Via Intestinal Sweet Taste Pathways

Young, Richard L.

doi:10.3389/fnins.2011.00023

Cited by 58 publications

(49 citation statements)

References 184 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Note that in this context, satiation refers to the processes involved in meal termination whereas satiety refers to the postprandial absence of hunger, which contributes to the determination of the interval between meals. Overall, release of these hormones depends on meal content and is broadly related to energy content but also depends on meal quality (Cummings & Overduin, 2007;Young, 2011). These hormones can act directly on receptors expressed by hypothalamic and/or brain stem neurons and/or indirectly on receptors expressed on vagus nerve terminals that project to the NTS.…”

Section: Humoral Inputsmentioning

confidence: 99%

Nicotinic Regulation of Energy Homeostasis

Zoli

Picciotto

2012

Nicotine & Tobacco Research

View full text Add to dashboard Cite

Introduction: The ability of nicotine, the primary psychoactive substance in tobacco smoke, to regulate appetite and body weight is one of the factors cited by smokers that prevents them from quitting and is the primary reason for smoking initiation in teenage girls. The regulation of feeding and metabolism by nicotine is complex, and recent studies have begun to identify nicotinic acetylcholine receptor (nAChR) subtypes and circuits or cell types involved in this regulation.

show abstract

Section: Humoral Inputsmentioning

confidence: 99%

Nicotinic Regulation of Energy Homeostasis

Zoli

Picciotto

2012

Nicotine & Tobacco Research

View full text Add to dashboard Cite

show abstract

“…It is been shown by Sutherland et al [26] and Yonug et al [27] that α-gustducin in rodents is expressed in small portion of L-cells (15%), but its density is higher in other enteroendocrine cells (brush cells 57%, 5-HT-containing enterochromaffin cells 27%). It have been shown that L cell exist distinct populations of L cells, and that glucose-sensitive L cells could be located in the upper intestine, with glucose-insensitive L cells located in the lower intestine [1].…”

Section: Discussionmentioning

confidence: 99%

“…Their result indicate that T1R3 may serve as the receptor for sweet perception in mice. Young [27] indicated that intestinal sweet taste molecules was dynamic regulation of expression and that levels of sweet taste molecule transcripts are modulated in the intestine by both luminal and metabolic factors. The present study, sensitive of sweet taste receptor to glucose may also be related to the difference of T1R3 expression level in the intestine from that from tongue although we did not observe this difference.…”

Section: Discussionmentioning

confidence: 99%

Dose-dependent effect of glucose on GLP-1 secretion involves sweet taste receptor in isolated perfused rat ileum [Rapid Communication]

Wang

Nian

et al. 2016

Endocr J

View full text Add to dashboard Cite

FOOD INTAKE results in the secretion of incretin hormones in the body, among which glucagon-like peptide 1 (GLP-1) and glucose-dependent insulin-releasing polypeptide (GIP) are responsible for 50%-70% insulin secretion after a meal [1]. Oral administration of glucose and fat results in two overlapping phases of GLP-1 secretion [2]. The early phase begins within minutes of a meal and continues for 30-60 min. The second phase causes prolonged secretion of GLP-1 at 1-3 h after a meal. This delayed phase of secretion involves the direct detection of luminal contents through enteroendocrine L-cells [1].Dietary nutrients, including carbohydrates, lipids, amino acids, and bile acids, can trigger GLP-1 release from particular intestinal endocrine L-cells. Specifically, glucose is a well-established stimulus for GLP-1 and GIP secretion in vivo. Studies suggested Dose-dependent effect of glucose on GLP-1 secretion involves sweet taste receptor in isolated perfused rat ileum Abstract. Luminal glucose is an important stimulus for glucagon-like peptide 1 (GLP-1) secretion from intestinal endocrine cells. However, the effects of luminal glucose concentration on GLP-1 secretion remain unknown. In this study, we investigated the effect of luminal glucose concentrations (3.5, 5, 10, 15, and 20 mmol/L) on GLP-1 secretion from isolated perfused rat ileum. Results showed that the perfusate glucose concentration dose-dependently stimulated GLP-1 secretion from isolated perfused rat ileum, which was eliminated by the sweet taste receptor inhibitor gurmarin (30 μg/mL), but not inhibited by phloridzin (1 mmol/L), a Na + -coupled glucose transporters inhibitor. We conclude that luminal glucose induced GLP-1 secretion from perfused rat ileum in a concentration-dependent manner. This secretion was mediated by sweet taste receptor transducing signal for GLP-1 release on the gut of rat.

show abstract

“…Intestinal glucose is absorbed primarily by two glucose transporters (GTs)-sodium dependent glucose co-transporter 1 (SGLT1) (10,11) and glucose transporter-2 (GLUT2) (12). Data derived from animal experiments indicate that intestinal glucose absorption is modulated, in large part, by intestinal sweet taste receptors (STRs), heterodimers of the G-protein-coupled receptors T1R2 and T1R3 (11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

“…Data derived from animal experiments indicate that intestinal glucose absorption is modulated, in large part, by intestinal sweet taste receptors (STRs), heterodimers of the G-protein-coupled receptors T1R2 and T1R3 (11)(12)(13). STRs, in the presence of intestinal sweet tastants, trigger increased expression of SGLT1 and GLUT2 to promote glucose absorption (14,15).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of intestinal glucose transporters after Roux-en-Y gastric bypass to prevent carbohydrate malabsorption

Nguyen

Debreceni

Bambrick

et al. 2014

Obesity

Self Cite

View full text Add to dashboard Cite

Objective: To determine the effect of Roux-en-Y gastric bypass (RYGB) on the expression of intestinal sweet taste receptors (STRs), glucose transporters (GTs), glucose absorption, and glycemia. Methods: Intestinal biopsies were collected for mRNA expression of STR (T1R2) and GTs (SGLT-1 and GLUT2) from 11 non-diabetic RYGB, 13 non-diabetic obese, and 11 healthy subjects, at baseline and following a 30 min small intestinal (SI) glucose infusion (30 g/150 ml water with 3 g 3-O-methyl-D-glucopyranose (3-OMG)). Blood glucose, plasma 3-OMG, and insulin were measured for 270 min. Results: In RYGB patients, expression of both GTs was 2-fold higher at baseline and after glucose infusion than those of morbidly obese or healthy subjects (P < 0.001). STR expressions were comparable amongst the groups. Peak plasma 3-OMG in both RYGB (r 5 0.69, P 5 0.01) and obese (r 5 0.72, P 5 0.005) correlated with baseline expression of SGLT-1, as was the case with peak blood glucose in RYGB subjects (r 5 0.69, P 5 0.02). Conclusions: The upregulated intestinal GTs in RYGB patients are associated with increased glucose absorption when glucose is delivered at a physiological rate, suggesting a molecular adaptation to prevent carbohydrate malabsorption from rapid intestinal transit after RYGB.

show abstract

Sensing Via Intestinal Sweet Taste Pathways

Cited by 58 publications

References 184 publications

Nicotinic Regulation of Energy Homeostasis

Nicotinic Regulation of Energy Homeostasis

Dose-dependent effect of glucose on GLP-1 secretion involves sweet taste receptor in isolated perfused rat ileum [Rapid Communication]

Upregulation of intestinal glucose transporters after Roux-en-Y gastric bypass to prevent carbohydrate malabsorption

Contact Info

Product

Resources

About