Metabolic responses to fructose-1,6-diphosphate in healthy subjects

Markov, Angel K.; Neely, William A.; Didlake, Ralph; Terry, Joe; Causey, Alan L.; Lehan, Patrick H.

doi:10.1053/meta.2000.6249

Cited by 19 publications

(14 citation statements)

References 28 publications

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“…The results of acute and short-term studies of fructose ingestion, ranging from periods of 4 hours to 6 days, indicate that when fructose is consumed in large amounts ranging from 30–50% of total calories, net fat oxidation is decreased and net carbohydrate oxidation is increased (Chong et al 2007, Couchepin et al 2008, Markov et al 2000, Schwarz et al 1989, Schwarz et al 1992a, Schwarz et al 1992b, Tappy et al 1986). However, the majority of these studies only examined the effects of consuming a single meal containing fructose, and those that examined the effects of multiple days of fructose consumption did not do so under energy-balanced conditions, but rather during consumption of 25–50% excess calories.…”

Section: Discussionmentioning

confidence: 99%

“…Previous investigations of the effects of fructose consumption on substrate utilization and energy expenditure are limited to acute or short-term studies (Chong et al 2007, Couchepin et al 2008, Markov et al 2000, Schwarz et al 1989, Schwarz et al 1992a, Schwarz et al 1992b, Tappy et al 1986). Our results from this 10 week study indicate that in overweight/obese adults, 40–72 years of age, sustained consumption of fructose-sweetened beverages, at 25% of energy requirements, leads to decreased net postprandial fat oxidation and increased net postprandial carbohydrate oxidation, similar to what has been observed in short-term studies.…”

Section: Introductionmentioning

confidence: 99%

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Consumption of fructose-sweetened beverages for 10 weeks reduces net fat oxidation and energy expenditure in overweight/obese men and women

et al. 2011

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Background/ObjectivesThe results of short-term studies in humans suggest that, compared with glucose, acute consumption of fructose leads to increased postprandial energy expenditure and carbohydrate oxidation and decreased postprandial fat oxidation. The objective of this study was to determine the potential effects of increased fructose consumption compared to isocaloric glucose consumption on substrate utilization and energy expenditure following sustained consumption and under energy-balanced conditions.Subjects/MethodsAs part of a parallel arm study, overweight/obese male and female subjects, 40–72 y, consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Energy expenditure and substrate utilization were assessed using indirect calorimetry at baseline and during the 10th week of intervention.ResultsConsumption of fructose, but not glucose, led to significant decreases of net postprandial fat oxidation and significant increases of net postprandial carbohydrate oxidation (P < 0.0001 for both). Resting energy expenditure decreased significantly from baseline values in subjects consuming fructose (P = 0.031) but not in those consuming glucose.ConclusionsIncreased consumption of fructose for 10 weeks leads to marked changes of postprandial substrate utilization including a significant reduction of net fat oxidation. In addition, we report that resting energy expenditure is reduced compared to baseline values in subjects consuming fructose-sweetened beverages for 10 weeks.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Consumption of fructose-sweetened beverages for 10 weeks reduces net fat oxidation and energy expenditure in overweight/obese men and women

et al. 2011

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“…It has been safely used in patients with myocardial damage (Munger et al, 1994), ischemic heart disease (Pasotti et al, 1989;Liu et al, 1998), ischemic stroke (Karaca et al, 2002), and during coronary artery bypass graft surgery (Riedel et al, 2004). It has also been found to be safe in trials with healthy volunteers in doses from 5 to 15 g (Ripari and Pieralisi, 1988;Markov et al, 2000). However, intravenous administration of F1,6BP has been shown to have an LD 50 in rats of 1,068 mg/kg (Nunes et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Fructose-1,6-Bisphosphate Has Anticonvulsant Activity in Models of Acute Seizures in Adult Rats

Lian¹,

Khan²,

Stringer³

2007

J. Neurosci.

110

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A variety of observations suggest that decreasing glycolysis and increasing levels of reduced glutathione, generated by metabolism of glucose through the pentose phosphate pathway, would have an anticonvulsant effect. Because fructose-1,6-bisphosphate (F1,6BP) shifts the metabolism of glucose from glycolysis to the pentose phosphate pathway, it was hypothesized to have anticonvulsant activity. The anticonvulsant activity of F1,6BP was determined in rat models of acute seizures induced by pilocarpine, kainic acid, or pentylenetetrazole. The efficacy of F1,6BP was compared with that of 2-deoxyglucose (2-DG; an inhibitor of glucose uptake and glycolysis), valproic acid (VPA), and the ketogenic diet. One hour before each convulsant, Sprague Dawley rats received either saline (as seizure controls), F1,6BP (0.25, 0.5 or 1 g/kg), 2-DG (0.25 or 0.5 g/kg), or VPA (0.3 g/kg). Additional animals received the ketogenic diet (starting at 20 or 60 d old). Time to seizure onset, seizure duration, and seizure score were measured in each group. F1,6BP had dose-dependent anticonvulsant activity in all three models, whereas VPA had partial efficacy. 2-DG was only effective in the pilocarpine model. The ketogenic diet had no effect in these models. F1,6BP was also partially effective when given at the first behavioral seizure after pilocarpine. Administration of sodium lactate, which bypasses the block in the glycolytic pathway, abolished the anticonvulsant activity of 2-DG in the pilocarpine model, but only decreased the efficacy of F1,6BP. These data demonstrate that F1,6BP has significant anticonvulsant efficacy.

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“…The protective role of FBP has been attributed to reduction of ATP loss [3,21] or regulation of glucose metabolism [24]. In organotypic slice cultures subjected to hypoxic conditions, FBP initiated a series of neuroprotective signals including PLC activation and increased activity of the ERK signaling pathway [13,28].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotection by fructose-1,6-bisphosphate involves ROS alterations via p38 MAPK/ERK

et al. 2004

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Metabolic responses to fructose-1,6-diphosphate in healthy subjects

Cited by 19 publications

References 28 publications

Consumption of fructose-sweetened beverages for 10 weeks reduces net fat oxidation and energy expenditure in overweight/obese men and women

Consumption of fructose-sweetened beverages for 10 weeks reduces net fat oxidation and energy expenditure in overweight/obese men and women

Fructose-1,6-Bisphosphate Has Anticonvulsant Activity in Models of Acute Seizures in Adult Rats

Neuroprotection by fructose-1,6-bisphosphate involves ROS alterations via p38 MAPK/ERK

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