Article (Scientific journals)
Effect of a high fructose diet on metabolic parameters in carriers for hereditary fructose intolerance.
Debray, François-Guillaume; Seyssel, Kevin; FADEUR, Marjorie et al.
2021In Clinical Nutrition, 40 (6), p. 4246-4254
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Keywords :
Fructose; Healthy carriers; Hereditary fructose intolerance; Insulin; Uric acid; Blood Glucose; Uric Acid; Fructose-Bisphosphate Aldolase; Glucose; Adult; Blood Glucose/metabolism; Cross-Over Studies; Diet, Carbohydrate Loading/adverse effects; Diet, Carbohydrate Loading/methods; Fasting/blood; Female; Fructose/administration & dosage; Fructose/adverse effects; Fructose Intolerance/blood; Fructose Intolerance/genetics; Fructose-Bisphosphate Aldolase/genetics; Glucose/administration & dosage; Glucose/adverse effects; Heterozygote; Humans; Hyperuricemia/etiology; Hyperuricemia/genetics; Insulin/blood; Insulin Resistance/genetics; Liver/metabolism; Male; Meals/physiology; Metabolic Syndrome/blood; Metabolic Syndrome/genetics; Postprandial Period; Uric Acid/blood; Diet, Carbohydrate Loading; Fasting; Fructose Intolerance; Hyperuricemia; Insulin Resistance; Liver; Meals; Metabolic Syndrome; Nutrition and Dietetics; Critical Care and Intensive Care Medicine
Abstract :
[en] ("[en] BACKGROUND & AIMS: Hyperuricemia is an independent risk factor for the metabolic syndrome and cardiovascular disease. We hypothesized that asymptomatic carriers for hereditary fructose intolerance (OMIM 22960) would have increased uric acid and altered component of the metabolic syndrome when exposed to fructose overfeeding. METHODS: Six heterozygotes for HFI (hHFI) and 6 controls (Ctrl) were studied in a randomized, controlled, crossover trial. Participants ingested two identical test meals containing 0.7 g kg-1 glucose and 0.7 g kg-1 fructose according to a cross-over design, once after a 7-day on a low fructose diet (LoFruD, <10 g/d) and on another occasion after 7 days on a high fructose diet (HiFruD, 1.4 g kg-1 day-1 fructose + 0.1 g kg-1 day-1 glucose). Uric acid, glucose, and insulin concentrations were monitored in fasting conditions and over 2 h postprandial, and insulin resistance indexes were calculated. RESULTS: HiFruD increased fasting uric acid (p < 0.05) and reduced fasting insulin sensitivity estimated by the homeostasis model assessment (HOMA) for insulin resistance (p < 0.05), in both groups. Postprandial glucose concentrations were not different between hHFI and Ctrl. However HiFruD increased postprandial plasma uric acid, insulin and hepatic insulin resistance index (HIRI) in hHFI only (all p < 0.05). CONCLUSIONS: Seven days of HiFruD increased fasting uric acid and slightly reduced fasting HOMA index in both groups. In contrast, HiFruD increased postprandial uric acid, insulin concentration and HIRI in hHFI only, suggesting that heterozygosity for pathogenic Aldolase B variants may confer an increased susceptibility to the effects of dietary fructose on uric acid and hepatic insulin sensitivity. This trial was registered at the U.S. Clinical Trials Registry as NCT03545581.","[en] ","")
Disciplines :
Endocrinology, metabolism & nutrition
Author, co-author :
Debray, François-Guillaume ;  Centre Hospitalier Universitaire de Liège - CHU > > Service de génétique
Seyssel, Kevin ;  Department of Biomedical Sciences, University of Lausanne, 1005 Lausanne, Switzerland
FADEUR, Marjorie ;  Centre Hospitalier Universitaire de Liège - CHU > > Service de diabétologie, nutrition, maladies métaboliques
Tappy, Luc ;  Department of Biomedical Sciences, University of Lausanne, 1005 Lausanne, Switzerland
Paquot, Nicolas ;  Centre Hospitalier Universitaire de Liège - CHU > > Service de diabétologie, nutrition, maladies métaboliques
Tran, Christel ;  Center for Molecular Diseases, Division of Genetic Medicine, University of Lausanne, Lausanne, Switzerland. Electronic address: christel.tran@chuv.ch
Language :
English
Title :
Effect of a high fructose diet on metabolic parameters in carriers for hereditary fructose intolerance.
Publication date :
2021
Journal title :
Clinical Nutrition
ISSN :
0261-5614
eISSN :
1532-1983
Publisher :
Churchill Livingstone, England
Volume :
40
Issue :
6
Pages :
4246-4254
Peer reviewed :
Peer Reviewed verified by ORBi
Funders :
ULiège - Université de Liège [BE]
UNIL - Université de Lausanne [CH]
Funding text :
We thank Valentine Rey and Nathalie Stefanoni (Department of Biomedical Sciences, University of Lausanne) for laboratory analysis. We sincerely thank Ariane Caris (dietician at the department of Medical Genetics, Metabolic Unit at the University Hospital of Liège) for having calculated dietary intake from dietary records. We also thank Andrea Superti-Furga for his critical and constructive review of the manuscript. Additionally, this is a study that was supported by the Fondation Raymond Berger , Switzerland and CT was supported by a "Pépinière" Grant form the University of Lausanne Faculty of Biology and Medicine , Switzerland. NP and MF were supported by a “ Fonds d'investissement de recherche scientifique ” Grant from the CHU of Liège.We thank Valentine Rey and Nathalie Stefanoni (Department of Biomedical Sciences, University of Lausanne) for laboratory analysis. We sincerely thank Ariane Caris (dietician at the department of Medical Genetics, Metabolic Unit at the University Hospital of Li?ge) for having calculated dietary intake from dietary records. We also thank Andrea Superti-Furga for his critical and constructive review of the manuscript. Additionally, this is a study that was supported by the Fondation Raymond Berger, Switzerland and CT was supported by a ?P?pini?re? Grant form the University of Lausanne Faculty of Biology and Medicine, Switzerland. NP and MF were supported by a ?Fonds d'investissement de recherche scientifique? Grant from the CHU of Li?ge.
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