Acute Fructose Administration Improves Oral Glucose Tolerance in Adults With Type 2 Diabetes

Moore, Mary Courtney; Mann, Samuel; Cherrington, Alan D.

doi:10.2337/diacare.24.11.1882

Cited by 108 publications

(81 citation statements)

References 32 publications

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“…These results are similar to our recent study (Heacock et al, 2002) in which we found that 10 g of supplemental fructose, when given with an MGTT (50 g carbohydrate from instant mashed potatoes), had no effect on the postprandial glycemic response. The lack of efficacy when fed with a meal in the present study, as compared with a free glucose beverage (Moore et al, 2000(Moore et al, , 2001, may be related to the effects of free glucose on the absorption of fructose (Hoekstra & van den Aker, 1996;Shi et al, 1997). Rats have a higher capacity for absorbing free fructose compared with the human.…”

Section: Discussionmentioning

confidence: 62%

Effects of a beverage containing an enzymatically induced-viscosity dietary fiber, with or without fructose, on the postprandial glycemic response to a high glycemic index food in humans

et al. 2003

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Objective: Dietary supplementation with guar gum or fructose has been reported to reduce the postprandial glycemic response to an oral glucose challenge. As a result of the poor palatability of most foods containing guar gum, a novel low-viscosity beverage with guar gum was developed that becomes viscous in vivo through an enzymatic induction. The primary study objective was to determine the effect of an amylase-induced viscosity (I-V) product, with or without supplemental fructose, on the postprandial glycemic response to a high glycemic index test meal in healthy nondiabetic subjects. Design: The study was a four-treatment, placebo-controlled, double-blind, randomized block protocol. Setting: The study was performed at Glycaemic Index Testing, Inc., Toronto, Ontario, Canada. Subjects: A total of 30 healthy nondiabetic volunteers (13 male, 17 female, mean7s.e.m. age of 5173 y and body mass index of 24.270.4 kg/m 2 ) participated in the study. Intervention: In the morning after an overnight fast, subjects participated in four 3-h meal glucose tolerance tests on separate occasions. The test meals contained 50 g of available carbohydrate from maltodextrin and white bread (control) or the same meal with either 5 g of guar gum (3.6 g galactomannan), 5 g of fructose, or 5 g of guar gum þ 5 g of fructose.Results: Treatments containing guar gum had a reduced (Po0.01) baseline-adjusted peak glucose response and incremental area under the glucose curve. In contrast to previous studies, fructose increased (Po0.05) the baseline-adjusted peak glucose concentration. Conclusions: Guar gum incorporated into an amylase I-V product provided a means to stabilize blood glucose levels by reducing the early phase excursion and then by appropriately maintaining the later phase excursion in healthy nondiabetic humans.

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Section: Discussionmentioning

confidence: 62%

Effects of a beverage containing an enzymatically induced-viscosity dietary fiber, with or without fructose, on the postprandial glycemic response to a high glycemic index food in humans

et al. 2003

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“…Type 2 diabetes is associated with impaired glucose tolerance and incomplete suppression of hepatic glucose production by hyperglycemia. These defects can be corrected, in part, by fructose administration (23,24), supporting a role for GK as a potential therapeutic target for type 2 diabetes. As a first step toward a novel therapeutic strategy for the control of glycemia in type 2 diabetes, our aim was to identify potent activators of GK that increase the affinity of liver cells for glucose and thereby lower the hepatic glucose threshold.…”

Section: Discussionmentioning

confidence: 95%

“…This mechanism enables rapid translocation of the enzyme to the cytoplasm in response to a rise in the extracellular concentration of glucose or fructose that occurs after a meal, resulting in a rapid increase in the rate of glucose phosphorylation (19). The role of this mechanism in regulating glucose metabolism is evident from the correlation between the rate of glucose phosphorylation and the free GK activity that is not bound to GKRP (19 -21) and from the stimulation of glucose disposal by fructose administration in vivo (22)(23)(24). Accordingly, it can be hypothesized that agents that cause either direct activation of GK or its dissociation from GKRP (25) are a potential strategy for stimulating hepatic glucose disposal in hyperglycemic conditions.…”

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confidence: 99%

Stimulation of Hepatocyte Glucose Metabolism by Novel Small Molecule Glucokinase Activators

et al. 2004

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Glucokinase (GK) has a major role in the control of blood glucose homeostasis and is a strong potential target for the pharmacological treatment of type 2 diabetes. We report here the mechanism of action of two novel and potent direct activators of GK: 6-[(3-isobutoxy-5-isopropoxybenzoyl)amino]nicotinic acid (GKA1) and 5-({3-isopropoxy-5-[2-(3-thienyl)ethoxy] benzoyl}amino)-1,3,4-thiadiazole-2-carboxylic acid (GKA2), which increase the affinity of GK for glucose by 4-and 11-fold, respectively. GKA1 increased the affinity of GK for the competitive inhibitor mannoheptulose but did not affect the affinity for the inhibitors palmitoylCoA and the endogenous 68-kDa regulator (GK regulatory protein [GKRP]), which bind to allosteric sites or to N-acetylglucosamine, which binds to the catalytic site. In hepatocytes, GKA1 and GKA2 stimulated glucose phosphorylation, glycolysis, and glycogen synthesis to a similar extent as sorbitol, a precursor of fructose 1-phosphate, which indirectly activates GK through promoting its dissociation from GKRP. Consistent with their effects on isolated GK, these compounds also increased the affinity of hepatocyte metabolism for glucose. GKA1 and GKA2 caused translocation of GK from the nucleus to the cytoplasm. This effect was additive with the effect of sorbitol and is best explained by a "glucose-like" effect of the GK activators in translocating GK to the cytoplasm. In conclusion, GK activators are potential antihyperglycemic agents for the treatment of type 2 diabetes through the stimulation of hepatic glucose metabolism by a mechanism independent of GKRP. Diabetes 53:535-541, 2004

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“…Clinical translation of these findings has shown that small doses of fructose decrease the postprandial blood glucose response to oral glucose in people with5 and without type 2 diabetes 6. Under chronic feeding conditions, fructose, in exchange for other carbohydrates, has further been shown to decrease HbA1c in systematic reviews and meta‐analyses of controlled feeding trials 7, 8.…”

Section: Introductionmentioning

confidence: 99%

The effect of small doses of fructose and allulose on postprandial glucose metabolism in type 2 diabetes: A double‐blind, randomized, controlled, acute feeding, equivalence trial

Noronha

Braunstein

Glenn

et al. 2018

Diabetes Obesity Metabolism

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AimTo assess and compare the effect of small doses of fructose and allulose on postprandial blood glucose regulation in type 2 diabetes.MethodsA double‐blind, multiple‐crossover, randomized, controlled, acute feeding, equivalence trial in 24 participants with type 2 diabetes was conducted. Each participant was randomly assigned six treatments separated by >1‐week washouts. Treatments consisted of fructose or allulose at 0 g (control), 5 g or 10 g added to a 75‐g glucose solution. A standard 75‐g oral glucose tolerance test protocol was followed with blood samples at −30, 0, 30, 60, 90 and 120 minutes. The primary outcome measure was plasma glucose incremental area under the curve (iAUC).ResultsAllulose significantly reduced plasma glucose iAUC by 8% at 10 g compared with 0 g (717.4 ± 38.3 vs. 777.5 ± 39.9 mmol × min/L, P = 0.015) with a linear dose response gradient between the reduction in plasma glucose iAUC and dose (P = 0.016). Allulose also significantly reduced several related secondary and exploratory outcome measures at 5 g (plasma glucose absolute mean and total AUC) and 10 g (plasma glucose absolute mean, absolute and incremental maximum concentration [Cmax], and total AUC) (P < .0125). There was no effect of fructose at any dose. Although allulose showed statistically significant reductions in plasma glucose iAUC compared with fructose at 5 g, 10 g and pooled doses, these reductions were within the pre‐specified equivalence margins of ±20%.ConclusionAllulose, but not fructose, led to modest reductions in the postprandial blood glucose response to oral glucose in individuals with type 2 diabetes. There is a need for long‐term randomized trials to confirm the sustainability of these improvements.

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Acute Fructose Administration Improves Oral Glucose Tolerance in Adults With Type 2 Diabetes

Cited by 108 publications

References 32 publications

Effects of a beverage containing an enzymatically induced-viscosity dietary fiber, with or without fructose, on the postprandial glycemic response to a high glycemic index food in humans

Effects of a beverage containing an enzymatically induced-viscosity dietary fiber, with or without fructose, on the postprandial glycemic response to a high glycemic index food in humans

Stimulation of Hepatocyte Glucose Metabolism by Novel Small Molecule Glucokinase Activators

The effect of small doses of fructose and allulose on postprandial glucose metabolism in type 2 diabetes: A double‐blind, randomized, controlled, acute feeding, equivalence trial

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