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

Foods ◽  
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.

Subcutaneous glucagon-like peptide-1 improves postprandial glycaemic control over a 3-week period in patients with early Type 2 diabetes

1998 ◽  
Vol 95 (3) ◽  
pp. 325-329 ◽  
Author(s):  
Jeannie F. TODD ◽  
C. Mark B. EDWARDS ◽  
Mohammad A. GHATEI ◽  
Hugh M. MATHER ◽  
Stephen R. BLOOM
Keyword(s):  
Type 2 Diabetes ◽  
Glycaemic Control ◽  
Plasma Glucose ◽  
Test Meal ◽  
Insulin Response ◽  
Standard Test ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
First Phase Insulin Response

1.Glucagon-like peptide-1 (7-36) amide (GLP-1) is released into the circulation after meals and is the most potent physiological insulinotropic hormone in man. GLP-1 has the advantages over other therapeutic agents for Type 2 diabetes of also suppressing glucagon secretion and delaying gastric emptying. One of the initial abnormalities of Type 2 diabetes is the loss of the first-phase insulin response, leading to postprandial hyperglycaemia. 2.To investigate the therapeutic potential of GLP-1 in Type 2 diabetes, six patients were entered into a 6-week, double-blind crossover trial during which each received 3 weeks treatment with subcutaneous GLP-1 or saline, self-administered three times a day immediately before meals. A standard test meal was given at the beginning and end of each treatment period. 3.GLP-1 reduced plasma glucose area under the curve (AUC) after the standard test meal by 58% (AUC, 0–240 ;min: GLP-1 start of treatment, 196±141 ;mmol·min-1·l-1; saline start of treatment, 469±124 ;mmol·min-1·l-1; F = 16.4, P< 0.05). The plasma insulin excursions were significantly higher with GLP-1 compared with saline over the initial postprandial 30 ;min, the time period during which the GLP-1 concentration was considerably elevated. The plasma glucagon levels were significantly lower over the 240-min postprandial period with GLP-1 treatment. The beneficial effects of GLP-1 on plasma glucose, insulin and glucagon concentrations were fully maintained for the 3-week treatment period. 4.We have demonstrated a significant improvement in postprandial glycaemic control with subcutaneous GLP-1 treatment. GLP-1 improves glycaemic control partially by restoring the first-phase insulin response and suppressing glucagon and is a potential treatment for Type 2 diabetes.

THE EFFECT OF URINARY GLUCOSE EXCRETION ON THE PLASMA GLUCOSE CLEARANCES AND PLASMA INSULIN RESPONSES TO INTRAVENOUS GLUCOSE LOADS IN UNANAESTHESIZED DOGS

1978 ◽  
Vol 87 (1) ◽  
pp. 133-138 ◽  
Author(s):  
J. J. Kaneko ◽  
D. Mattheeuws ◽  
R. P. Rottiers ◽  
J. Van Der Stock ◽  
A. Vermeulen
Keyword(s):  
Plasma Glucose ◽  
Insulin Response ◽  
Immunoreactive Insulin ◽  
Glucose Load ◽  
Urinary Glucose Excretion ◽  
Intravenous Glucose ◽  
K Value ◽  
Urinary Glucose ◽  
Glucose Clearance ◽  
Glucose Excretion

ABSTRACT The effect of urinary glucose excretion on the plasma glucose clearance and insulin response to varying sizes of glucose loads was studied in normal unanaesthesized dogs. Glucose loads ranging from 0.15 to 1.25 g/kg b.w. were infused intravenously in a standard time period of 30 seconds. Plasma glucose and plasma immunoreactive insulin (IRI) concentrations were determined during one-hour after infusion. All urine excreted during the one-hour was collected by a catheterization and bladder wash-out procedure. The urinary glucose excretion was expressed as the percent of the glucose load. The urinary glucose excretion varied directly with the size of the glucose load and ranged from minimal to 12 %. This would indicate that urinary losses play a considerable role proportionate to the degree of hyperglycaemia above the renal threshold. Thus, urinary loss of glucose must be recognized as an important factor influencing the plasma glucose clearance and hence the plasma IRI response. A glucose load of 0.5 g/kg b.w. given in 30 seconds with the k-value calculated between 15–45 min would minimize the influence of urinary loss and provide more accurate plasma clearance values.

Glucose tolerance and insulin secretion after adrenalectomy in mice made obese with gold thioglucose

1996 ◽  
Vol 148 (3) ◽  
pp. 391-398 ◽  
Author(s):  
S C Blair ◽  
I D Caterson ◽  
G J Cooney
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Insulin Release ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
The Body ◽  
Obese Mice ◽  
Glucose Load ◽  
Intravenous Glucose ◽  
Gold Thioglucose

Abstract The effect of adrenalectomy (ADX) on glucose tolerance and insulin secretion was examined in conscious mice made obese by a single injection of gold thioglucose (GTG). To facilitate such a study a chronic jugular catheter was implanted into the mice at the time of performing the ADX or sham-ADX. One week after ADX, the body weight (GTG-obese+sham-ADX, 35·6 ± 0·6 g; GTG-obese+ADX, 33·1 ± 0·6 g; P<0·05) and glycogen content of the liver (GTG-obese+sham-ADX, 2·4 ± 0·2 μmol/liver; GTG-obese+ADX, 1·6 ± 0·1 μmol/liver; P<0·05) of GTG-injected mice were reduced. Plasma glucose concentrations, in both the overnight fasted state and in response to an intravenous glucose load were also reduced following ADX of GTG-obese mice, but not to the level of the sham-ADX control mice. However, ADX completely normalized plasma insulin concentrations in both the basal state and also in response to a glucose load, as indicated by the finding that the integrated insulin secretory response of the ADX GTG-obese mice was not different from that of sham-ADX control mice (control+sham-ADX, 192 ± 5 min.μU/ml; GTG-obese+ADX, 196 ± 10 min.μU/ml). The effects of ADX on carbohydrate metabolism were not restricted to GTG-injected mice, as ADX of control mice decreased fasting plasma glucose levels and reduced liver glycogen and plasma insulin concentrations. The normalization of insulin release in ADX GTG-obese mice occurred while these mice were still obese and glucose intolerant. This suggests that the decreased insulin release was not due solely to an ADX-induced improvement in insulin sensitivity and/or weight loss. Removal of central glucocorticoid effects on the parasympathetic stimulation of insulin release may play a role in the reduced insulin release observed after ADX of obese and control mice, although peripheral effects of glucocorticoid deficiency on glycogen synthesis in the liver may also influence whole animal glucose homeostasis. Journal of Endocrinology (1996) 148, 391–398

Does a glucose load inhibit hepatic sugar output? C14 glucose studies in eviscerated dogs

1959 ◽  
Vol 197 (1) ◽  
pp. 60-62 ◽  
Author(s):  
Robert Steele ◽  
Jonathan S. Bishop ◽  
Rachmiel Levine
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Alternative Explanation ◽  
Specific Activity ◽  
The Body ◽  
Glucose Load ◽  
Hepatic Glucose Output ◽  
Minute Amount ◽  
Hepatic Glucose ◽  
Glucose Output

A sequence of changes in plasma glucose specific activity is observed in intact dogs when a large amount of C12 glucose is injected intravenously following the tagging of the circulating glucose by injection of a minute amount of C14 glucose. Similar changes are observed when the same procedure is applied to eviscerated dogs in which the plasma glucose concentration is being maintained by a continuous infusion of C12 glucose, this infusion being continued unchanged after the C12 glucose load is given. These results show that inhibition of hepatic glucose output is not the only or the necessary explanation for the cessation in the exponential fall of plasma glucose specific activity which is seen in the intact dog following an intravenous C12 glucose load. An alternative explanation of the effect is offered which is based on the slowness of mixing of the injected C12 glucose load with a part of the body glucose pool.

Low Vitamin K Intake Effects on Glucose Tolerance in Rats

1999 ◽  
Vol 69 (1) ◽  
pp. 27-31 ◽  
Author(s):  
Sakamoto ◽  
Wakabayashi ◽  
Sakamoto
Keyword(s):  
Glucose Tolerance ◽  
Vitamin K ◽  
Plasma Glucose ◽  
Insulin Response ◽  
Glucose Load ◽  
Intravenous Glucose ◽  
Intravenous Glucose Tolerance ◽  
Glucose Tolerance Tests ◽  
Early Insulin Response ◽  
Intravenous Glucose Tolerance Tests

To investigate the effects of vitamin K (VK) on pancreatic function, intravenous glucose tolerance tests were performed in rats fed with and without low VK diet (inclucing less than 20% required vitamin K1). Plasma glucose and immuno-reactive insulin (IRI) were determined. It was found that at 0 min., plasma glucose and IRI levels in low VK group were slightly less than in the control (glucose, 204.5 ± 21.7 vs. 229 ± 19.6 mg/dl, IRI, 6.6 ± 1.3 vs. 9.3 ± 1.8 ng/ml mean ± SEM). At 3 min. after glucose administration, plasma glucose was higher (391.8 ± 25.6 vs. 371.8 ± 18.7 mg/dl) and IRI, lower (11.8 ± 2.1 vs. 18.2 ± 3.6 ng/ml) in the low VK group. The disappearance rate of plasma glucose in the low VK group at 5–10 min. was significantly less than in the control (6.7 ± 2.2 vs. 11.9 ± 1.8 mg/ dl/min.). Incremental IRI area at 0 to 5 min. in the low VK group is less than in the control (15.2 ± 4.4 vs. 25.0 ± 9.1 ng/ml/min.), but at 5–60 min. and 0–60 min., it was found to be significantly higher compared to the control (210.3 ± 55.2 vs. 32.5 ± 47.1 ng/ml/min. at 5–60 min.). Dietary low VK intake would thus appear to induce a tendency of poor early insulin response, and late hyperinsulinemia to the glucose load in rats.

scholarly journals Intragastric administration of the bitter tastant quinine lowers the glycemic response to a nutrient drink without slowing gastric emptying in healthy men

2020 ◽  
Vol 318 (2) ◽  
pp. R263-R273 ◽  
Author(s):  
Vida Bitarafan ◽  
Penelope C. E. Fitzgerald ◽  
Tanya J. Little ◽  
Wolfgang Meyerhof ◽  
Karen L. Jones ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Gastric Emptying ◽  
Energy Intake ◽  
Plasma Glucose ◽  
Postprandial Blood Glucose ◽  
Intragastric Administration ◽  
Glycemic Response ◽  
Experimental Conditions ◽  
Double Blind ◽  
Healthy Men

The rate of gastric emptying and the release of gastrointestinal (GI) hormones are major determinants of postprandial blood-glucose concentrations and energy intake. Preclinical studies suggest that activation of GI bitter-taste receptors potently stimulates GI hormones, including glucagon-like peptide-1 (GLP-1), and thus may reduce postprandial glucose and energy intake. We evaluated the effects of intragastric quinine on the glycemic response to, and the gastric emptying of, a mixed-nutrient drink and the effects on subsequent energy intake in healthy men. The study consisted of 2 parts: part A included 15 lean men, and part B included 12 lean men (aged 26 ± 2 yr). In each part, participants received, on 3 separate occasions, in double-blind, randomized fashion, intragastric quinine (275 or 600 mg) or control, 30 min before a mixed-nutrient drink ( part A) or before a buffet meal ( part B). In part A, plasma glucose, insulin, glucagon, and GLP-1 concentrations were measured at baseline, after quinine alone, and for 2 h following the drink. Gastric emptying of the drink was also measured. In part B, energy intake at the buffet meal was quantified. Quinine in 600 mg (Q600) and 275 mg (Q275) doses alone stimulated insulin modestly ( P < 0.05). After the drink, Q600 and Q275 reduced plasma glucose and stimulated insulin ( P < 0.05), Q275 stimulated GLP-1 ( P < 0.05), and Q600 tended to stimulate GLP-1 ( P = 0.066) and glucagon ( P = 0.073) compared with control. Quinine did not affect gastric emptying of the drink or energy intake. In conclusion, in healthy men, intragastric quinine reduces postprandial blood glucose and stimulates insulin and GLP-1 but does not slow gastric emptying or reduce energy intake under our experimental conditions.

scholarly journals Diurnal trends in responses of blood plasma concentrations of glucose, insulin, and C-peptide following high- and low-fat meals and their relation to fat metabolism in healthy middle-aged volunteers

1997 ◽  
Vol 77 (4) ◽  
pp. 523-535 ◽  
Author(s):  
David L. Frape ◽  
Norman R. Williams ◽  
A. J. Scriven ◽  
Christopher R. Palmer ◽  
Kathryn O'Sullivan ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Fat Metabolism ◽  
Plasma Concentrations ◽  
Insulin Response ◽  
Latin Squares ◽  
Postprandial Blood Glucose ◽  
High Fat ◽  
Middle Aged ◽  
C Peptide ◽  
Fat Meal

An experiment was conducted in twelve healthy middle-aged volunteers, six of each sex, with a mean BMI of 27kg/m2 to detect differences between morning and afternoon in postprandial blood glucose, insulin and C-peptide concentrations. These responses were measured following the consumption of isoenergetic meals that were high or low in fat content, at breakfast and at lunch. Over 4d each subject received the high-carbohydrate (L, 5·5 g mixed fat/meal) and moderately high-fat (M, 33 g mixed fat/meal) breakfasts and lunches, in three combinations (LL, MM, LM), or they fasted at breakfast time and received a moderately high-fat lunch (NM), in three Latin squares. Each evening a standard meal was given. Plasma glucose, insulin and C-peptide responses were greater following L than M meals and within both MM and LL treatments insulin and C-peptide responses were greater following breakfast than following lunch. The incremental C-peptide response to a fatty lunch following a fast at breakfast time (NM) was similar to that to a fatty breakfast, but the incremental insulin response for the same comparison was marginally lower at lunch (P=0·06). The relationship of C-peptide and insulin concentrations was assessed. Plasma glucose response to a fatty lunch was increased by a fatty breakfast. The relationships of these metabolic events with fat metabolism are discussed.

Early insulin response after food intake in geese

1992 ◽  
Vol 263 (4) ◽  
pp. R782-R784
Author(s):  
H. Karmann ◽  
N. Rideau ◽  
T. Zorn ◽  
A. Malan ◽  
Y. Le Maho
Keyword(s):  
Insulin Secretion ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Insulin Level ◽  
Food Ingestion ◽  
Standard Meal ◽  
Cephalic Phase ◽  
Early Insulin Response ◽  
Freely Moving

Plasma glucose and insulin levels were measured in chronically catheterized, freely moving, undisturbed geese, which were offered a free standard meal after an overnight fast. The insulin level markedly rose within the first minute after the start of food ingestion, whereas plasma glucose did not increase. This early insulin response was not correlated with the size of the meal. In contrast, both postabsorptive insulin response and plasma glucose changes were dependent on meal size. When a small amount of food (2-6 g) was eaten, insulin returned to basal level within 30 min, whereas plasma glucose remained unchanged. Larger meals (15-20 g) maintained plasma insulin at a higher level and induced a sustained rise of plasma glucose. These results indicate that there is a cephalic phase of insulin secretion at the beginning of the meal in birds as previously described in mammals.

scholarly journals Interaction of fish oil and a glucocorticoid on metabolic responses to an oral glucose load in healthy human subjects

2006 ◽  
Vol 95 (2) ◽  
pp. 267-272 ◽  
Author(s):  
Jacques Delarue ◽  
Chang-Hong Li ◽  
Richard Cohen ◽  
Charlotte Corporeau ◽  
Brigitte Simon
Keyword(s):  
Fish Oil ◽  
Plasma Glucose ◽  
Insulin Response ◽  
Substrate Oxidation ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
Healthy Human ◽  
Chain Pufa ◽  
Long Chain

Compared with saturated fat, n-3 long-chain PUFA-rich fish oil improves insulin sensitivity in rats. We studied whether n-3 long-chain PUFA could prevent insulin resistance induced by dexamethasone (a glucocorticoid) in healthy human volunteers. A group of eight subjects was studied twice after a 2d dexamethasone treatment, before and after a 3-week supplementation with fish oil (providing daily doses of 1·1g 20:5n-3 and 0·7g 22:6n-3). The subjects were studied during the basal state and over the 6h following an oral glucose load (1g/kg). Plasma glucose fluxes were traced with [6,6-2H2]glucose and [13C]glucose (naturally 13C-enriched corn glucose). Substrate oxidation was obtained from indirect calorimetry. Following fish oil supplementation, plasma glucose fluxes and substrate oxidation were maintained despite a 17% reduction (P<0·05) in the area under the curve of plasma insulin response, suggesting an insulin-sensitizing effect.

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