Effects of Fructose Infusion on Lactate and Uric Acid Metabolism

ExtractAfter the infusion of fructose, 0.25 g/kg body wt, the mean peak plasma uric acid lerel was 5.4 0.7 ( S E M ) mg/100 ml in six normal children and was not significantly increased compared with that of the mean basal kalue of 4.1 0.5 mg/100 ml. The mean blood inorganic phosphate ( P , ) levels were significantly less than the mean fasting value after fructose. Blood glucose. lactic acid, and fructose levels were significantly increased after fructose, but serum magnesium levels did not change.In two patients with hereditary fructose intolerance ( H F I ) the peak blood uric acid levels were 12.1 and 7.6 mg/100 ml. respectively, after fructose. In both patients the blood glucose concentrations decreased 69 and 26 mg/100 ml below the fasting levels after fructose. The serum P i level decreased 2.3 and 1.2 mg/100 ml below fasting values, decrements greater than the mean decrement in serum P, of 0.8 * 0.2 mg/100 ml which occurred in six normal children.The mean uric acid excretion, expressed as milligrams per mg urinary creatinine, was 0.6 i 0.1 ( S E M I before fructose in the normal children and increased significantly to 1.0 0.1 mg/mg creatinine after fructose. In two patients with HFI the uric acid excretion increased four-to fivefold after fructose administration; the increased uric acid excretion in HFI exceeded that of normal children.In three patients with galactosemia. increases in blood uric acid levels after galactose ingestion were similar to those in normal children after fructose, but less than those in patients with HFI after fructose. The serum P , levels decreased less in galactosemic patients after galactose administration than in patients with HFI after fructose infusion.These studies support the hypothesis that fructose-induced hyperuricemia results from degradation of adenosine monophosphate. This effect appears to be specific for fructose. The lack of hyperuricemia in galactosemia patients after galactose ingestion may be explained by the observation that galactose is phosphorylated more slowly than fructose. SpeculationFructose administration in individuals predisposed to hyperuricemia and gout may induce urate overproduction by decreasing intrahepatic P i and ATP content and ultimately lead to enhanced nucleotide catabolism. The pathogenesis of increased urate production in glycogen storage disease, type 1, may be similar to that proposed for fructose-induced hyperuricemia.

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“…accompanied by a marked uricosuria in normal children. A similar response has been noted in normal adults (44). In contrast.…”

Section: Discussionsupporting

confidence: 85%

“…Our f~ndings emphasize the phosphate, galactose, and erythrocyte galactose-I-P (GAL-I-P) after the ingestion of 50 g galactose in three patients with galactosemia. previous observations (24,44) that a higher total dose given over a brief period of time is required for the hyperuricemic effect of fructose in normal subjects.…”

Section: Discussionmentioning

confidence: 81%

Fructose-induced Hyperuricemia: Observations in Normal Children and in Patients with Hereditary Fructose Intolerance and Galactosemia

Kogut

Roe

et al. 1975

Pediatr Res

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“…The fate of ingested fructose may also depend on coingested nutrients. For instance, infusing physiological concentrations of fructose to fed rats and humans increases serum glucose and lactate levels without affecting hepatic glycogen accumulation (53,54). However, when fructose is infused with glucose, which stimulates insulin secretion, marked glycogen accumulation occurs (55).…”

Section: Intermediary Fructose Metabolismmentioning

confidence: 99%

Fructose metabolism and metabolic disease

Hannou

Haslam

McKeown

et al. 2018

Journal of Clinical Investigation

405

356

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“…However, an excess of fructose floods the glycolytic pathway with lipogenic precursors (glycerol-3-phosphate, acetyl-co-A) by bypassing the regulated step in the pathway catalysed by the enzyme phosphofructokinase (Underwood and Newsholme, 1965;Mayes, 1993). Fructose increases the production of lactate by an increased conversion of pyruvate by the enzyme lactic dehydrogenase (Sahebjami and Scalettar, 1971).…”

Section: Fructose and Metabolic Flexibilitymentioning

confidence: 99%

Obesity and energy balance: is the tail wagging the dog?

Wells¹,

Siervo²

2011

Eur J Clin Nutr

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The scientific study of obesity has been dominated throughout the twentieth century by the concept of energy balance. This conceptual approach, based on fundamental thermodynamic principles, states that energy cannot be destroyed, and can only be gained, lost or stored by an organism. Its application in obesity research has emphasised excessive appetite (gluttony), or insufficient physical activity (sloth), as the primary determinants of excess weight gain, reflected in current guidelines for obesity prevention and treatment. This model cannot explain why weight accumulates persistently rather than reaching a plateau, and underplays the effect of variability in dietary constituents on energy and intermediary metabolism. An alternative model emphasises the capacity of fructose and fructose-derived sweeteners (sucrose, high-fructose corn syrup) to perturb cellular metabolism via modification of the adenosine monophosphate (AMP)/adenosine triphosphate (ATP) ratio, activation of AMP kinase and compensatory mechanisms, which favour adipose tissue accretion and increased appetite while depressing physical activity. This conceptual model implicates chronic hyperinsulinaemia in the presence of a paradoxical state of 'cellular starvation' as a key driver of the metabolic modifications inducing chronic weight gain. We combine evidence from in vitro and in vivo experiments to formulate a perspective on obesity aetiology that emphasises metabolic flexibility and dietary composition rather than energy balance. Using this model, we question the direction of causation of reported associations between obesity and sleep duration or childhood growth. Our perspective generates new hypotheses, which can be tested to improve our understanding of the current obesity epidemic, and to identify novel strategies for prevention or treatment. (2011) 65, 1173-1189; doi:10.1038/ejcn.2011.132; published online 20 July 2011 European Journal of Clinical NutritionKeywords: fructose; obesity; metabolism; energy balance; metabolic flexibility IntroductionThe scientific study of obesity has been dominated throughout the twentieth century by the concept of energy balance. This conceptual approach, based on fundamental thermodynamic principles, states that energy cannot be destroyed, and can only be gained, lost or stored by an organism (Hess, 1838;von Helmholtz, 1847). Its application in obesity research has emphasised excessive appetite, or insufficient physical activity, as the primary determinants of the modification of energy balance leading to excess weight gain (Prentice and Jebb, 1995), reflected in current protocols for obesity prevention and treatment. As we review below, this model cannot explain why weight accumulates persistently in individuals, rather than reaching a plateau when weight gain re-establishes the balance between energy intake and expenditure. The energy balance approach also underplays the effect of particular dietary components (for example, carbohydrates, amino-acids and fatty acids) on energy metabolism and fuel oxidati...

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Effects of Fructose Infusion on Lactate and Uric Acid Metabolism

Cited by 94 publications

References 15 publications

Fructose-induced Hyperuricemia: Observations in Normal Children and in Patients with Hereditary Fructose Intolerance and Galactosemia

Fructose-induced Hyperuricemia: Observations in Normal Children and in Patients with Hereditary Fructose Intolerance and Galactosemia

Fructose metabolism and metabolic disease

Obesity and energy balance: is the tail wagging the dog?

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