Sweet taste: Effect on cephalic phase insulin release in men

Sensory stimulation from foods elicits cephalic phase responses, which facilitate digestion and nutrient assimilation. One such response, cephalic-phase insulin release (CPIR), enhances glucose tolerance. Little is known about the chemosensory mechanisms that activate CPIR. We studied the contribution of the sweet taste receptor (T1r2+T1r3) to sugar-induced CPIR in C57BL/6 (B6) and T1r3 knockout (KO) mice. First, we measured insulin release and glucose tolerance following oral (i.e., normal ingestion) or intragastric (IG) administration of 2.8 M glucose. Both groups of mice exhibited a CPIR following oral but not IG administration, and this CPIR improved glucose tolerance. Second, we examined the specificity of CPIR. Both mouse groups exhibited a CPIR following oral administration of 1 M glucose and 1 M sucrose but not 1 M fructose or water alone. Third, we studied behavioral attraction to the same three sugar solutions in short-term acceptability tests. B6 mice licked more avidly for the sugar solutions than for water, whereas T1r3 KO mice licked no more for the sugar solutions than for water. Finally, we examined chorda tympani (CT) nerve responses to each of the sugars. Both mouse groups exhibited CT nerve responses to the sugars, although those of B6 mice were stronger. We propose that mice possess two taste transduction pathways for sugars. One mediates behavioral attraction to sugars and requires an intact T1r2+T1r3. The other mediates CPIR but does not require an intact T1r2+T1r3. If the latter taste transduction pathway exists in humans, it should provide opportunities for the development of new treatments for controlling blood sugar.

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Palatability and Dietary Restraint: Effect on Cephalic Phase Insulin Release in Women

Physiology & Behavior ◽

10.1016/0031-9384(96)00043-1 ◽

1996 ◽

Vol 60 (2) ◽

pp. 575-579

Author(s):

K Teff

Keyword(s):

Insulin Release ◽

Dietary Restraint ◽

Cephalic Phase

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Cephalic phase responses to sweet taste

American Journal of Clinical Nutrition ◽

10.1093/ajcn/65.3.737 ◽

1997 ◽

Vol 65 (3) ◽

pp. 737-743 ◽

Cited By ~ 67

Author(s):

L Abdallah ◽

M Chabert ◽

J Louis-Sylvestre

Keyword(s):

Sweet Taste ◽

Cephalic Phase

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Glucose elicits cephalic-phase insulin release in mice by activating KATP channels in taste cells

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00433.2016 ◽

2017 ◽

Vol 312 (4) ◽

pp. R597-R610 ◽

Cited By ~ 23

Author(s):

John I. Glendinning ◽

Yonina G. Frim ◽

Ayelet Hochman ◽

Gabrielle S. Lubitz ◽

Anthony J. Basile ◽

...

Keyword(s):

Signaling Pathway ◽

Insulin Release ◽

Katp Channels ◽

Glucose Sensing ◽

Oral Glucose ◽

Β Cells ◽

Oral Stimulation ◽

Cephalic Phase ◽

Taste Cells ◽

A Subunit

The taste of sugar elicits cephalic-phase insulin release (CPIR), which limits the rise in blood glucose associated with meals. Little is known, however, about the gustatory mechanisms that trigger CPIR. We asked whether oral stimulation with any of the following taste stimuli elicited CPIR in mice: glucose, sucrose, maltose, fructose, Polycose, saccharin, sucralose, AceK, SC45647, or a nonmetabolizable sugar analog. The only taste stimuli that elicited CPIR were glucose and the glucose-containing saccharides (sucrose, maltose, Polycose). When we mixed an α-glucosidase inhibitor (acarbose) with the latter three saccharides, the mice no longer exhibited CPIR. This revealed that the carbohydrates were hydrolyzed in the mouth, and that the liberated glucose triggered CPIR. We also found that increasing the intensity or duration of oral glucose stimulation caused a corresponding increase in CPIR magnitude. To identify the components of the glucose-specific taste-signaling pathway, we examined the necessity of Calhm1, P2X2+P2X3, SGLT1, and Sur1. Among these proteins, only Sur1 was necessary for CPIR. Sur1 was not necessary, however, for taste-mediated attraction to sugars. Given that Sur1 is a subunit of the ATP-sensitive K+ channel (KATP) channel and that this channel functions as a part of a glucose-sensing pathway in pancreatic β-cells, we asked whether the KATP channel serves an analogous role in taste cells. We discovered that oral stimulation with drugs known to increase (glyburide) or decrease (diazoxide) KATP signaling produced corresponding changes in glucose-stimulated CPIR. We propose that the KATP channel is part of a novel signaling pathway in taste cells that mediates glucose-induced CPIR.

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ATP-sensitive K+ channel-independent glucose action in rat pancreatic beta-cell

AJP Cell Physiology ◽

10.1152/ajpcell.1994.266.3.c622 ◽

1994 ◽

Vol 266 (3) ◽

pp. C622-C627 ◽

Cited By ~ 55

Author(s):

T. Aizawa ◽

Y. Sato ◽

F. Ishihara ◽

N. Taguchi ◽

M. Komatsu ◽

...

Keyword(s):

Glucose Metabolism ◽

Beta Cell ◽

Phospholipase C ◽

Insulin Release ◽

Islet Cells ◽

Pancreatic Beta Cell ◽

Cytosolic Calcium ◽

Sweet Taste ◽

K Channel ◽

Glucose Molecule

The nature of ATP-sensitive K+ (K+ATP) channel-independent, insulinotropic action of glucose was investigated using non-glucose-primed pancreatic islets. When the beta-cell was depolarized with K+, glucose dose dependently stimulated insulin release despite inhibition of the K+ATP channel closure by diazoxide. K+ depolarization could be replaced with BAY K 8644, a calcium channel agonist. Prior fasting of rats and lowering ambient temperature greatly suppressed glucose oxidation and utilization by the islet cells and abolished insulin release in response to high glucose alone. However, under these conditions, the K+ATP channel-independent, glucose-induced insulin release was clearly demonstrable. p-Nitrophenyl-alpha-D-glucopyranoside (sweet taste inhibitor) but not its beta-isomer, neomycin (phospholipase C inhibitor) and staurosporine (C kinase blocker) inhibited the K+ATP channel-independent, insulinotropic action of glucose. For the K+ATP channel-independent glucose-induced insulin release 1) elevation of cytosolic calcium is required, 2) minute glucose metabolism is enough, if glucose metabolism is necessary, and 3) direct recognition of glucose molecule, phospholipase C, and protein kinase C appear to be involved.

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Vagotomy Suppresses Cephalic Phase Insulin Release in Sheep

Experimental Physiology ◽

10.1111/j.1469-445x.1999.01872.x ◽

1999 ◽

Vol 84 (3) ◽

pp. 559-569 ◽

Cited By ~ 10

Author(s):

C. B. Herath ◽

G. W. Reynolds ◽

D. D. S. Mackenzie ◽

S. R. Davis ◽

P. M. Harris

Keyword(s):

Insulin Release ◽

Cephalic Phase

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Satiety, Taste and the Cephalic Phase: A Crossover Designed Pilot Study into Taste and Glucose Response

Foods ◽

10.3390/foods9111578 ◽

2020 ◽

Vol 9 (11) ◽

pp. 1578

Author(s):

Thanyathorn Sae iab ◽

Robin Dando

Keyword(s):

Plasma Glucose ◽

Test Meal ◽

Insulin Response ◽

Sweet Taste ◽

The Body ◽

Postprandial Blood Glucose ◽

Caloric Content ◽

Glycemic Response ◽

Glucose Load ◽

Cephalic Phase

The glycemic response produced by a food depends on both the glycemic index of the food itself, and on how the body reacts to the food as it is consumed and digested, in turn dependent on sensory cues. Research suggests that taste stimulation can induce the cephalic phase insulin response before food has reached the digestion, priming the body for an incoming glucose load. This glycemic response can consequently affect the amount of food consumed in a subsequent meal. The aim of this study was to investigate the effects on satiety of four preloads that differed in caloric content and sensory properties, in a small group of female and male participants (n = 10). Water, sucrose, sucralose, and maltodextrin were used to represent 4 different conditions of the preload, with or without energy, and with or without sweet taste. Individual plasma glucose concentrations were sampled at baseline, 45 min after consuming the preload, and after consuming an ad-libitum test meal. Hunger, fullness, desire to eat, and thoughts of food feeling were assessed every 15 min using visual analog scales. Results in male participants when comparing two solutions of equal caloric content, maltodextrin and sucrose, showed that plasma glucose concentration spiked in the absence of taste input (p = 0.011). Maltodextrin, while providing calories does not have the sweet taste that can serve to trigger cephalic phase insulin release to attenuate an incoming glucose load, and was accompanied by significantly greater change in feelings of satiety than with the other preloads. Despite the difference in postprandial blood glucose, the energy consumed in the test meal across the treatments was not significantly different in either males or females. Results highlight the importance of taste in stimulating the body for the efficient and effective glucose homeostasis.

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Sham feeding-induced cephalic phase insulin release in the rat

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1982.242.4.e280 ◽

1982 ◽

Vol 242 (4) ◽

pp. E280-E285 ◽

Cited By ~ 18

Author(s):

H. R. Berthoud ◽

B. Jeanrenaud

Keyword(s):

Insulin Release ◽

Intravenous Administration ◽

Hepatic Glucose Production ◽

Insulin Response ◽

Glucose Production ◽

Glucose Disposal ◽

Adrenergic Stimulation ◽

Sham Feeding ◽

Cephalic Phase ◽

Atropine Methyl Nitrate

The effect of the cephalic phase of food ingestion on plasma insulin and glucagon concentration was assessed in the sham-feeding rat, bearing chronically implanted gastric drainage fistulas. It was found that continuous sham feeding produced a significant and phasic peripheral insulin response in the absence of any significant changes of glycemia. The response was almost completely blocked by prior intravenous administration of 2 mg/kg of atropine methyl nitrate and potentiated by prior intravenous administration of 1.0 or 2.5 mg/kg of phentolamine. In spite of the larger insulin response after phentolamine, there was no hypoglycemia detected. Furthermore, continuous sham feeding did not produce a significant glucagon response, whereas real feeling did. The results demonstrate that cholinergic insulin release is triggered phasically by continuous ingestion of familiar food and that this insulin response is inhibited by an alpha-adrenergic sympathetic tone. It is further concluded that the increased glucose disposal produced by the neurally released insulin is not counteracted by a concomitant glucagon response or by direct adrenergic stimulation of hepatic glucose production.

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Sweet-taste receptors, low-energy sweeteners, glucose absorption and insulin release

British Journal Of Nutrition ◽

10.1017/s0007114510002540 ◽

2010 ◽

Vol 104 (10) ◽

pp. 1415-1420 ◽

Cited By ~ 60

Author(s):

Andrew G. Renwick ◽

Samuel V. Molinary

Keyword(s):

Insulin Release ◽

Taste Receptor ◽

Sweet Taste ◽

Glucose Absorption ◽

Enteroendocrine Cells ◽

Low Energy ◽

Taste Receptors ◽

Sweet Taste Receptors

The present review explores the interactions between sweeteners and enteroendocrine cells, and consequences for glucose absorption and insulin release. A combination of in vitro,in situ, molecular biology and clinical studies has formed the basis of our knowledge about the taste receptor proteins in the glucose-sensing enteroendocrine cells and the secretion of incretins by these cells. Low-energy (intense) sweeteners have been used as tools to define the role of intestinal sweet-taste receptors in glucose absorption. Recent studies using animal and human cell lines and knockout mice have shown that low-energy sweeteners can stimulate intestinal enteroendocrine cells to release glucagon-like peptide-1 and glucose-dependent insulinotropic peptide. These studies have given rise to major speculations that the ingestion of food and beverages containing low-energy sweeteners may act via these intestinal mechanisms to increase obesity and the metabolic syndrome due to a loss of equilibrium between taste receptor activation, nutrient assimilation and appetite. However, data from numerous publications on the effects of low-energy sweeteners on appetite, insulin and glucose levels, food intake and body weight have shown that there is no consistent evidence that low-energy sweeteners increase appetite or subsequent food intake, cause insulin release or affect blood pressure in normal subjects. Thus, the data from extensive in vivo studies in human subjects show that low-energy sweeteners do not have any of the adverse effects predicted by in vitro,in situ or knockout studies in animals.

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