Taste of glucose elicits cephalic-phase insulin release in mice

2018 ◽  
Vol 192 ◽  
pp. 200-205 ◽  
Author(s):  
John I. Glendinning ◽  
Gabrielle S. Lubitz ◽  
Sarah Shelling
Keyword(s):  
Insulin Release ◽  
Cephalic Phase

Sweet taste: Effect on cephalic phase insulin release in men

1995 ◽  
Vol 57 (6) ◽  
pp. 1089-1095 ◽  
Author(s):  
Karen L. Teff ◽  
John Devine ◽  
Karl Engelman
Keyword(s):  
Insulin Release ◽  
Sweet Taste ◽  
Cephalic Phase

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

2017 ◽  
Vol 312 (4) ◽  
pp. R597-R610 ◽  
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.

scholarly journals Vagotomy Suppresses Cephalic Phase Insulin Release in Sheep

1999 ◽  
Vol 84 (3) ◽  
pp. 559-569 ◽  
Author(s):  
C. B. Herath ◽  
G. W. Reynolds ◽  
D. D. S. Mackenzie ◽  
S. R. Davis ◽  
P. M. Harris
Keyword(s):  
Insulin Release ◽  
Cephalic Phase

Sham feeding-induced cephalic phase insulin release in the rat

1982 ◽  
Vol 242 (4) ◽  
pp. E280-E285 ◽  
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.

A role for insulin in cephalic phase of postprandial thermogenesis in dogs

1988 ◽  
Vol 254 (5) ◽  
pp. E625-E632 ◽  
Author(s):  
P. Diamond ◽  
J. LeBlanc
Keyword(s):  
Causal Relationship ◽  
Insulin Release ◽  
Respiratory Quotient ◽  
Plasma Insulin ◽  
Control Experiment ◽  
Second Phase ◽  
O2 Consumption ◽  
Cephalic Phase ◽  
Postprandial Thermogenesis ◽  
Peak Increase

The influence of insulin in the cephalic phase of postprandial thermogenesis was investigated in dogs. O2 consumption (VO2) and respiratory quotient (RQ) were continuously monitored 1 h before and 2 h after a 1,015-kcal meal during a control, an atropine, or a pancreatic-denervation experiment. A first phase (cephalic phase) in VO2 increase, lasting at least 50 min, followed by a second phase (digestive phase) were found in the control experiment. During both the atropine and pancreatic-denervation experiment, the first phase of VO2 was inhibited by 52%. The second phase was completely abolished with atropine, whereas it remained comparable to the control in the case of pancreatic denervation. A peak increase for insulin (70 microU/ml over 0 time) was observed 2 min after the onset of feeding in control. It was followed after 25 min by a second increase related to changes in glycemia. Maximal rises of norepinephrine (NE) and epinephrine corresponded to 215 and 120 pg/ml above basal values at 2 min in control experiment. During both atropine and pancreatic denervation the cephalic phase of insulin release was suppressed and the NE increase was inhibited by congruent to 65%. During the digestive phase pancreatic denervation caused an increase in plasma insulin comparable to that of the control, whereas atropine produced no such effect. It is suggested that the cephalic phase of postprandial thermogenesis is mediated through a causal relationship between insulin and NE release.

scholarly journals A single night of partial sleep loss impairs fasting insulin sensitivity but does not affect cephalic phase insulin release in young men

2015 ◽  
Vol 25 (1) ◽  
pp. 5-10 ◽  
Author(s):  
Jonathan Cedernaes ◽  
Lauri Lampola ◽  
Emil K. Axelsson ◽  
Lisanne Liethof ◽  
Sara Hassanzadeh ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Insulin Release ◽  
Young Men ◽  
Sleep Loss ◽  
Fasting Insulin ◽  
Cephalic Phase ◽  
Single Night

scholarly journals Sugar-induced cephalic-phase insulin release is mediated by a T1r2+T1r3-independent taste transduction pathway in mice

2015 ◽  
Vol 309 (5) ◽  
pp. R552-R560 ◽  
Author(s):  
John I. Glendinning ◽  
Sarah Stano ◽  
Marlena Holter ◽  
Tali Azenkot ◽  
Olivia Goldman ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Insulin Release ◽  
Taste Receptor ◽  
Sensory Stimulation ◽  
Sweet Taste ◽  
Transduction Pathway ◽  
Nutrient Assimilation ◽  
Cephalic Phase ◽  
Taste Transduction ◽  
New Treatments

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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