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Background: High fructose intake increases blood lactate, triglyceride and uric acid concentrations. Uric acid may contribute to insulin resistance and dyslipidemia in the general population. In patients with hereditary fructose intolerance fructose consumption is associated with acute hypoglycemia, renal tubular acidosis, and hyperuricemia.
Objective: We investigated whether asymptomatic carriers for hereditary fructose intolerance (HFI) would have a higher sensitivity to adverse effects of fructose than the general population.
Design: Eight subjects heterozygous for HFI (hHFI; 4 males, 4 females) and eight controls received for 7 days a low fructose diet and on the eighth day ingested a test meal calculated to provide 25% of basal energy requirement containing labeled fructose (13C fructose 0.35 g/kg), protein (0.21 g/kg) and lipid (0.22 g/kg). Total fructose oxidation, total endogenous glucose production (by 6,6-2H2-glucose dilution), carbohydrate and lipid oxidation, lipids, uric acid, lactate, creatinine, urea and amino acids were monitored for 6 hours.
Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Basic Science
Hereditary Fructose Intolerance
University of Lausanne
Published on BioPortfolio: 2016-12-02T16:38:22-0500
This study aimed to examine metabolic response to a short-term fructose enriched diet in carriers for hereditary fructose intolerance compared to controls. Effects of fructose coffees will...
Fructose is the principal carbohydrate in fruits and is added to many food products. This 5 carbon sugar is associated with a number of ill effects, like promotion of high triglycerides,pr...
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Inherited abnormalities of fructose metabolism, which include three known autosomal recessive types: hepatic fructokinase deficiency (essential fructosuria), hereditary fructose intolerance, and hereditary fructose-1,6-diphosphatase deficiency. Essential fructosuria is a benign asymptomatic metabolic disorder caused by deficiency in fructokinase, leading to decreased conversion of fructose to fructose-1-phosphate and alimentary hyperfructosemia, but with no clinical dysfunction; may produce a false-positive diabetes test.
An autosomal recessive fructose metabolism disorder due to deficient fructose-1-phosphate aldolase (EC 188.8.131.52) activity, resulting in accumulation of fructose-1-phosphate. The accumulated fructose-1-phosphate inhibits glycogenolysis and gluconeogenesis, causing severe hypoglycemia following ingestion of fructose. Prolonged fructose ingestion in infants leads ultimately to hepatic failure and death. Patients develop a strong distaste for sweet food, and avoid a chronic course of the disease by remaining on a fructose- and sucrose-free diet.
An enzyme that catalyzes the conversion of D-fructose 1,6-bisphosphate and water to D-fructose 6-phosphate and orthophosphate. EC 184.108.40.206.
Passage of food (sometimes in the form of a test meal) through the gastrointestinal tract as measured in minutes or hours. The rate of passage through the intestine is an indicator of small bowel function.
An allosteric enzyme that regulates glycolysis and gluconeogenesis by catalyzing the transfer of a phosphate group from ATP to fructose-6-phosphate to yield fructose-2,6-bisphosphate, an allosteric effector for the other 6-phosphofructokinase, PHOSPHOFRUCTOKINASE-1. Phosphofructokinase-2 is bifunctional: the dephosphorylated form is a kinase and the phosphorylated form is a phosphatase that breaks down fructose-2,6-bisphosphate to yield fructose-6-phosphate.
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Chronic kidney disease (CKD), also known as chronic renal disease, is a progressive loss in renal function over a period of months or years. The symptoms of worsening kidney function are non-specific, and might include feeling generally unwell and experi...