scholarly journals The cephalic phase insulin response to nutritive and low-calorie sweeteners in solid and beverage form

2017 ◽  
Vol 181 ◽  
pp. 100-109 ◽  
Author(s):  
Jaapna Dhillon ◽  
Janice Y. Lee ◽  
Richard D. Mattes
1999 ◽  
Vol 69 (2) ◽  
pp. 395-401 ◽  
Author(s):  
J. Rushen ◽  
S. Robert ◽  
C. Farmer

AbstractTo understand the mechanism underlying the effect of high-fibre diets on feeding motivation and stereotypic behaviour in pigs, non-pregnant gilts were given either concentrate or a high-fibre diet based on oat hulls and blood samples were assayed for cortisol, glucose, insulin and free fatty acids. The duration of eating was much longer for gilts on the high-fibre diet than gilts given concentrates. Concentrations of cortisol increased with food delivery and this was most pronounced with the concentrate diet. Concentrations of free fatty acids decreased before feeding and those of glucose and insulin decreased temporarily immediately after feeding began. The diet had no marked effect on these changes, although the decrease for insulin was less evident for the concentrate diet. As feeding continued, free fatty acid concentrations decreased, while concentrations of insulin and glucose increased. The increase in glucose and insulin was fastest with the concentrate diet, although post-feeding peak values did not differ. Postprandial cortisol and free fatty acid concentrations did not differ between diets. There was no evidence of a pre-prandial cephalic phase insulin or glucose response to feeding in the gilts although concentrations of both hormones decreased immediately after the gilts began to eat. The high-fibre diet tended to delay the peak glucose and insulin response to meals, suggesting that the reduced feeding motivation following consumption of high-fibre diets does not involve the same mechanism as the increased satiety following increased energy intake. As well as reducing the occurrence of ster eoty pies, high-fibre diets decrease cortisol concentrations at feeding.


Foods ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1578
Author(s):  
Thanyathorn Sae iab ◽  
Robin Dando

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.


1982 ◽  
Vol 242 (4) ◽  
pp. E280-E285 ◽  
Author(s):  
H. R. Berthoud ◽  
B. Jeanrenaud

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.


1980 ◽  
Vol 5 ◽  
pp. 127-131 ◽  
Author(s):  
H.R. Berthoud ◽  
D.A. Bereiter ◽  
B. Jeanrenaud

2018 ◽  
Vol 5 (3) ◽  
pp. 85-90 ◽  
Author(s):  
Wellington Santana da Silva ◽  
Caroline Buss ◽  
Nicolas Wiernsperger ◽  
Eliete Bouskela ◽  
Luiz Guilherme Kraemer-Aguia

1990 ◽  
Vol 258 (2) ◽  
pp. R523-R530 ◽  
Author(s):  
H. R. Berthoud ◽  
T. L. Powley

To define the vagal circuitry mediating the cephalic phase insulin response (CPIR), this reflex was measured in conscious, freely moving rats that had previously undergone selective abdominal vagotomies that spared different columnar subpopulations of dorsal motor nucleus of the vagus (dmnX) neurons. The CPIR was defined as an increase of plasma insulin from basal at 2 min after the start of ingestion. The CPIR measured in peripheral blood after chow ingestion was reliable and significant (P less than 0.05) in rats with all branches intact, +24.9 +/- 5.1 microU/ml (+130% increase from basal); rats with only the two gastric branches and the hepatic branch intact, +27.0 +/- 3.5 microU/ml (+153%); and rats with only the hepatic branch intact, +13.5 +/- 4.8 microU/ml (+188%). No significant response occurred in animals with only the two celiac branches intact, +1.8 +/- 1.8 microU/ml (+15%) or in those with none of the branches intact, +3.9 +/- 3.3 microU/ml (+21%). The CPIRs measured in portal vein blood were generally larger but showed the same pattern across groups. Plasma glucose measurements of portal vein blood indicated that with chow ingestion no significant absorption had occurred by 2 min, whereas with either milk or glucose intake absorption did occur. Subsequent bilateral electrical cervical vagal stimulation-induced insulin and glucagon responses in the same animals under anesthesia showed the same branch dependency. It is concluded that the CPIR is mediated by the two gastric and the hepatic branches but not the two celiac vagal branches. The perikarya of the preganglionics innervating the pancreatic B-cells are contained within a large pool occupying the two medial columns of the dmnX.


2019 ◽  
Vol 109 (4) ◽  
pp. 1051-1063
Author(s):  
Nathalie Weltens ◽  
Inge Depoortere ◽  
Jan Tack ◽  
Lukas Van Oudenhove

ABSTRACT Background The endocannabinoid system (ECS) is considered a key player in the neurophysiology of food reward. Animal studies suggest that the ECS stimulates the sensory perception of food, thereby increasing its incentive-motivational and/or hedonic properties and driving consumption, possibly via interactions with metabolic hormones. However, it remains unclear to what extent this can be extrapolated to humans. Objective We aimed to investigate the effect of oral Δ9-tetrahydrocannabinol (THC) on subjective and metabolic hormone responses to visual food stimuli and food intake. Methods Seventeen healthy subjects participated in a single-blinded, placebo-controlled, 2 × 2 crossover trial. In each of the 4 visits, subjective “liking” and “wanting” ratings of high- and low-calorie food images were acquired after oral THC or placebo administration. The effect on food intake was quantified in 2 ways: via ad libitum oral intake (half of the visits) and intragastric infusion (other half) of chocolate milkshake. Appetite-related sensations and metabolic hormones were measured at set time points throughout each visit. Results THC increased “liking” (P = 0.031) and “wanting” ratings (P = 0.0096) of the high-calorie, but not the low-calorie images, compared with placebo. Participants consumed significantly more milkshake after THC than after placebo during oral intake (P = 0.0005), but not intragastric infusion, of milkshake. Prospective food consumption ratings during the food image paradigm were higher after THC than after placebo (P = 0.0039). THC also increased plasma motilin (P = 0.0021) and decreased octanoylated ghrelin (P = 0.023) concentrations before milkshake consumption (i.e., in both oral intake and intragastric infusion test sessions), whereas glucagon-like peptide 1 responses to milkshake intake were attenuated by THC during both oral (P = 0.0002) and intragastric (P = 0.0055) administration. Conclusions These findings suggest that the ECS drives food intake by interfering with anticipatory, cephalic phase, and metabolic hormone responses. This trial was registered at clinicaltrials.gov as NCT02310347.


1980 ◽  
Vol 238 (4) ◽  
pp. E336-E340 ◽  
Author(s):  
H. R. Berthoud ◽  
E. R. Trimble ◽  
E. G. Siegel ◽  
D. A. Bereiter ◽  
B. Jeanrenaud

The ability of saccharin, in comparison with glucose and tap water, to elicit glycemia-independent neurally mediated insulin secretion was investigated in chronically catheterized, freely moving rats. Plasma glucose and insulin concentrations were measured continuously from venous blood with a sampling resolution of one per minute. In normal rats, 1 ml of 0.15% saccharin caused a significant rapid rise in peripheral plasma insulin levels lasting up to 5 min, without significant changes in glycemia. Tap water alone also induced a transient elevation in insulinemia but was much smaller than the saccharin-induced response. In streptozotocin diabetic rats bearing intrahepatic, presumably denervated islet isografts, these rapid insulin responses to oral saccharin and tap water stimulation were completely abolished, whereas the early insulin response to intravenous glucose was decreased by only about 30%. These results are consistent with the concept of gustatory and other oral sensory signals acting as triggers for neurally mediated insulin release.


Metabolism ◽  
1996 ◽  
Vol 45 (2) ◽  
pp. 168-173 ◽  
Author(s):  
L.J. Karhunen ◽  
R.I. Lappalainen ◽  
L.K. Niskanen ◽  
A.K. Turpeinen ◽  
M.I.J. Uusitupa

1985 ◽  
Vol 249 (6) ◽  
pp. E639-E645 ◽  
Author(s):  
F. Bellisle ◽  
J. Louis-Sylvestre ◽  
F. Demozay ◽  
D. Blazy ◽  
J. Le Magnen

Insulinemia and glycemia were measured at a 1-min interval at the hour of a lunch meal in human subjects. When no food was presented to naive subjects (n = 4), cyclic oscillations of insulinemia were found (period, 12-20 min; amplitude, 2.8-10.3 microU/ml). It is proposed that these spontaneous oscillations must be taken into consideration when evaluating the insulin response on cephalic contact with food stimuli; they might otherwise constitute a source of artifacts. Four subjects were then submitted to a series of four test meals scheduled at a 1-wk interval. Although their prandial glycemia remained comparable with preprandial values for the first 16 min of the meals, insulinemia often exhibited early peaks (within a few min after meal onset) whose amplitude appeared related to palatability conditions. Evidence suggests that the insulin peaks triggered by cephalic stimulation are Pavlovian reflexes that become conditioned to the test situation. A typical neuroendocrine response to alimentary frustration is also described. The results are discussed in perspective with animal works, in terms of the effects of neuroendocrine events on feeding behavior.


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