Influence of oral glucose ingestion on splanchnic glucose and gluconeogenic substrate metabolism in man

Diabetes ◽  
1975 ◽  
Vol 24 (5) ◽  
pp. 468-475 ◽  
Author(s):  
P. Felig ◽  
J. Wahren ◽  
R. Hendler
Keyword(s):  
Oral Glucose ◽  
Substrate Metabolism ◽  
Glucose Ingestion ◽  
Gluconeogenic Substrate

Abnormal Regulation of Venous Alanine after Glucose Ingestion in Myotonic Dystrophy

1985 ◽  
Vol 68 (2) ◽  
pp. 151-157 ◽  
Author(s):  
Richard T. Moxley ◽  
William Kingston ◽  
Robert C. Griggs
Keyword(s):  
Amino Acids ◽  
Glucose Tolerance ◽  
Myotonic Dystrophy ◽  
Normal Glucose Tolerance ◽  
Oral Glucose ◽  
Oral Glucose Tolerance Testing ◽  
Glucose Ingestion ◽  
Normal Glucose ◽  
Normal Males ◽  
Slight Rise

1. The concentration of amino acids in whole blood was measured before and during standard 5 h oral glucose tolerance testing in six male patients with myotonic dystrophy and five normal males. The plasma levels of insulin and glucose were also determined. 2. From 90 to 240 min after glucose ingestion there was a striking decline in venous alanine concentration in the patients with myotonic dystrophy in contrast to a slight rise in alanine in the normal group. 3. The patients displayed normal glucose tolerance, and there was a sustained fall in the venous concentration of the insulin-sensitive amino acids comparable with that seen in the normal controls. However, the patients showed a threefold increase of plasma insulin after glucose. 4. These data indicate an abnormal regulation of alanine in myotonic dystrophy which may be the result of an alteration in muscle synthesis of this amino acid. This defect in alanine synthesis may be due to a decreased availability of intracellular pyruvate caused by the insulin resistance that exists in these patients.

Effects of acute α2-blockade on insulin action and secretion in humans

1998 ◽  
Vol 274 (1) ◽  
pp. E57-E64 ◽  
Author(s):  
Andrea Natali ◽  
Amalia Gastaldelli ◽  
Alfredo Quiñones Galvan ◽  
Anna Maria Sironi ◽  
Demetrio Ciociaro ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Energy Expenditure ◽  
Plasma Insulin ◽  
Time Course ◽  
Resting Energy Expenditure ◽  
Oral Glucose ◽  
Cardiac Work ◽  
C Peptide ◽  
Glucose Ingestion ◽  
Resting Energy

We tested whether acute α2-blockade affects insulin secretion, glucose and fat metabolism, thermogenesis, and hemodynamics in humans. During a 5-h epinephrine infusion (50 ng ⋅ min−1 ⋅ kg−1) in five volunteers, deriglidole, a selective α2-receptor inhibitor, led to a more sustained rise in plasma insulin and C-peptide levels (+59 ± 14 vs. +28 ± 6, and +273 ± 18 vs. +53 ± 14 pM, P < 0.01 vs. placebo) despite a smaller rise in plasma glucose (+0.90 ± 0.4 vs. +1.5 ± 0.3 mM, P < 0.01). Another 10 subjects were studied in the postabsorptive state and during a 4-h hyperglycemic (+4 mM) clamp, coupled with the ingestion of 75 g of glucose at 2 h. In the postabsorptive state, hepatic glucose production, resting energy expenditure, and plasma insulin, free fatty acid (FFA), and potassium concentrations were not affected by acute α2-blockade. Hyperglycemia elicited a biphasic rise in plasma insulin (to a peak of 140 ± 24 pM), C-peptide levels (1,520 ± 344 pM), and insulin secretion (to 410 ± 22 pmol/min); superimposed glucose ingestion elicited a further twofold rise in insulin and C-peptide levels, and insulin secretion. However, α2-blockade failed to change these secretory responses. Fasting blood β-hydroxybutyrate and glycerol and plasma FFA and potassium concentrations all declined with hyperglycemia; time course and extent of these changes were not affected by α2-blockade. Resting energy expenditure (+25 vs. +16%, P < 0.01) and external cardiac work (+28% vs. +19%, P < 0.01) showed larger increments after α2-blockade. We conclude that acute α2-blockade in humans 1) prevents epinephrine-induced inhibition of insulin secretion, 2) does not potentiate basal or intravenous- or oral glucose-induced insulin release, 3) enhances thermogenesis, and 4) increases cardiac work.

scholarly journals Fructose Consumption Contributes to Hyperinsulinemia in Adolescents With Obesity Through a GLP-1–Mediated Mechanism

2019 ◽  
Vol 104 (8) ◽  
pp. 3481-3490 ◽  
Author(s):  
Alfonso Galderisi ◽  
Cosimo Giannini ◽  
Michelle Van Name ◽  
Sonia Caprio
Keyword(s):  
Glucose Tolerance ◽  
Mixed Model ◽  
Linear Mixed Model ◽  
Cell Function ◽  
Insulin Response ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Double Blind ◽  
Obesity And Diabetes ◽  
Glucose Ingestion

Abstract Context The consumption of high-fructose beverages is associated with a higher risk for obesity and diabetes. Fructose can stimulate glucagon-like peptide 1 (GLP-1) secretion in lean adults, in the absence of any anorexic effect. Objective We hypothesized that the ingestion of glucose and fructose may differentially stimulate GLP-1 and insulin response in lean adolescents and adolescents with obesity. Design We studied 14 lean adolescents [four females; 15.9 ± 1.6 years of age; body mass index (BMI), 21.8 ± 2.2 kg/m2] and 23 adolescents with obesity (five females; 15.1 ± 1.6 years of age; BMI, 34.5 ± 4.6 kg/m2). Participants underwent a baseline oral glucose tolerance test to determine their glucose tolerance and estimate insulin sensitivity and β-cell function [oral disposition index (oDIcpep)]. Eligible subjects received, in a double-blind, crossover design, 75 g of glucose or fructose. Plasma was obtained every 10 minutes for 60 minutes for the measures of glucose, insulin, and GLP-1 (radioimmunoassay) and glucose-dependent insulinotropic polypeptide (GIP; ELISA). Incremental glucose and hormone levels were compared between lean individuals and those with obesity by a linear mixed model. The relationship between GLP-1 increment and oDIcpep was evaluated by regression analysis. Results Following the fructose challenge, plasma glucose excursions were similar in both groups, yet the adolescents with obesity exhibited a greater insulin (P &lt; 0.001) and GLP-1 (P &lt; 0.001) increase than did their lean peers. Changes in GIP were similar in both groups. After glucose ingestion, the GLP-1 response (P &lt; 0.001) was higher in the lean group. The GLP-1 increment during 60 minutes from fructose drink was correlated with a lower oDIcpep (r2 = 0.22, P = 0.009). Conclusion Fructose, but not glucose, ingestion elicits a higher GLP-1 and insulin response in adolescents with obesity than in lean adolescents. Fructose consumption may contribute to the hyperinsulinemic phenotype of adolescent obesity through a GLP-1–mediated mechanism.

Oral glucose ingestion attenuates exercise-induced activation of 5′-AMP-activated protein kinase in human skeletal muscle

2006 ◽  
Vol 342 (3) ◽  
pp. 949-955 ◽  
Author(s):  
Thorbjorn C.A. Akerstrom ◽  
Jesper B. Birk ◽  
Ditte K. Klein ◽  
Christian Erikstrup ◽  
Peter Plomgaard ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Human Skeletal Muscle ◽  
Oral Glucose ◽  
Glucose Ingestion ◽  
Exercise Induced ◽  
Amp Activated Protein Kinase

scholarly journals Green tea extract does not affect exogenous glucose appearance but reduces insulinemia with glucose ingestion in exercise recovery

2016 ◽  
Vol 121 (6) ◽  
pp. 1282-1289 ◽  
Author(s):  
Brian J. Martin ◽  
Chris McGlory ◽  
Martin J. MacInnis ◽  
Mary K. Allison ◽  
Stuart M. Phillips ◽  
...  
Keyword(s):  
Green Tea ◽  
Green Tea Extract ◽  
Constant Infusion ◽  
Oral Glucose ◽  
Exercise Recovery ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
Glucose Kinetics ◽  
Glucose Ingestion ◽  
Tea Extract

We reported that supplementation with green tea extract (GTE) lowered the glycemic response to an oral glucose load following exercise, but via an unknown mechanism (Martin BJ, MacInnis MJ, Gillen JB, Skelly LE, Gibala MJ. Appl Physiol Nutr Metab 41: 1057–1063, 2016. Here we examined the effect of supplementation with GTE on plasma glucose kinetics on ingestion of a glucose beverage during exercise recovery. Eleven healthy, sedentary men (21 ± 2 yr old; body mass index = 23 ± 4 kg/m2, peak O2 uptake = 38 ± 7 ml·kg−1·min−1; means ± SD) ingested GTE (350 mg) or placebo (PLA) thrice daily for 7 days in a double-blind, crossover design. In the fasted state, a primed constant infusion of [U-13C6]glucose was started, and 1 h later, subjects performed a graded exercise test (25 W/3 min) on a cycle ergometer. Immediately postexercise, subjects ingested a 75-g glucose beverage containing 2 g of [6,6-2H2]glucose, and blood samples were collected every 10 min for 3 h of recovery. The rate of carbohydrate oxidation was lower during exercise after GTE vs. PLA (1.26 ± 0.34 vs. 1.48 ± 0.51 g/min, P = 0.04). Glucose area under the curve (AUC) was not different between treatments after drink ingestion (GTE = 1,067 ± 133 vs. PLA = 1,052 ± 91 mM/180 min, P = 0.91). Insulin AUC was lower after GTE vs. PLA (5,673 ± 2,153 vs. 7,039 ± 2,588 µIU/180 min, P = 0.05), despite similar rates of glucose appearance (GTE = 0.42 ± 0.16 vs. PLA = 0.43 ± 0.13 g/min, P = 0.74) and disappearance (GTE = 0.43 ± 0.14 vs. PLA = 0.44 ± 0.14 g/min, P = 0.57). We conclude that short-term GTE supplementation did not affect glucose kinetics following ingestion of an oral glucose load postexercise; however, GTE was associated with attenuated insulinemia. These findings suggest GTE lowers the insulin required for a given glucose load during postexercise recovery, which warrants further mechanistic studies in humans.

Oral glucose intake inhibits hypothalamic neuronal activity more effectively than glucose infusion

2007 ◽  
Vol 293 (3) ◽  
pp. E754-E758 ◽  
Author(s):  
Paul A. M. Smeets ◽  
Solrun Vidarsdottir ◽  
Cees de Graaf ◽  
Annette Stafleu ◽  
Matthias J. P. van Osch ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Glucose Solution ◽  
Normal Weight ◽  
Glucose Infusion ◽  
Transient Signal ◽  
Oral Glucose ◽  
Bold Signal ◽  
Healthy Humans ◽  
Glucose Intake ◽  
Glucose Ingestion

We previously showed that hypothalamic neuronal activity, as measured by the blood oxygen level-dependent (BOLD) functional MRI signal, declines in response to oral glucose intake. To further explore the mechanism driving changes in hypothalamic neuronal activity in response to an oral glucose load, we here compare hypothalamic BOLD signal changes subsequent to an oral vs. an intravenous (iv) glucose challenge in healthy humans. Seven healthy, normal-weight men received four interventions in random order after an overnight fast: 1) ingestion of glucose solution (75 g in 300 ml) or 2) water (300 ml), and 3) iv infusion of 40% glucose solution (0.5 g/kg body wt, maximum 35 g) or 4) infusion of saline (0.9% NaCl, equal volume). The BOLD signal was recorded as of 8 min prior to intervention (baseline) until 30 min after. Glucose infusion was associated with a modest and transient signal decline in the hypothalamus. In contrast, glucose ingestion was followed by a profound and persistent signal decrease despite the fact that plasma glucose levels were almost threefold lower than in response to iv administration. Accordingly, glucose ingestion tended to suppress hunger more than iv infusion ( P < 0.1). We infer that neural and endocrine signals emanating from the gastrointestinal tract are critical for the hypothalamic response to nutrient ingestion.

scholarly journals Diminished glucagon suppression after β-cell reduction is due to impaired α-cell function rather than an expansion of α-cell mass

2011 ◽  
Vol 300 (4) ◽  
pp. E717-E723 ◽  
Author(s):  
Juris J. Meier ◽  
Sandra Ueberberg ◽  
Simone Korbas ◽  
Stephan Schneider
Keyword(s):  
Insulin Treatment ◽  
Cell Function ◽  
Cell Mass ◽  
Glucagon Secretion ◽  
Pancreatic Tissue ◽  
Oral Glucose ◽  
Inverse Association ◽  
Β Cell ◽  
Glucose Ingestion ◽  
Glucagon Suppression

Impaired suppression of glucagon levels after oral glucose or meal ingestion is a hallmark of type 2 diabetes. Whether hyperglucagonemia after a β-cell loss results from a functional upregulation of glucagon secretion or an increase in α-cell mass is yet unclear. CD-1 mice were treated with streptozotocin (STZ) or saline. Pancreatic tissue was collected after 14, 21, and 28 days and examined for α- and β-cell mass and turnover. Intraperitoneal (ip) glucose tolerance tests were performed at day 28 as well as after 12 days of subcutaneous insulin treatment, and glucose, insulin, and glucagon levels were determined. STZ treatment led to fasting and post-challenge hyperglycemia ( P < 0.001 vs. controls). Insulin levels increased after glucose injection in controls ( P < 0.001) but were unchanged in STZ mice ( P = 0.36). Intraperitoneal glucose elicited a 63.1 ± 4.1% glucagon suppression in control mice ( P < 0.001), whereas the glucagon suppression was absent in STZ mice ( P = 0.47). Insulin treatment failed to normalize glucagon levels. There was a significant inverse association between insulin and glucagon levels after ip glucose ingestion ( r2 = 0.99). β-Cell mass was reduced by ∼75% in STZ mice compared with controls ( P < 0.001), whereas α-cell mass remained unchanged ( P > 0.05). α-Cell apoptosis (TUNEL) and replication (Ki67) were rather infrequently noticed, with no significant differences between the groups. These studies underline the importance of endogenous insulin for the glucose-induced suppression of glucagon secretion and suggest that the insufficient decline in glucagon levels after glucose administration in diabetes is primarily due to a functional loss of intraislet inhibition of α-cell function rather than an expansion of α-cell mass.

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