Effect of a high fructose diet on metabolic parameters in carriers for hereditary fructose intolerance
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 overf...
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| Veröffentlicht in: | Clinical nutrition (Edinburgh, Scotland) Scotland), 2021-06, Vol.40 (6), p.4246-4254 |
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| creator | Debray, François-Guillaume Seyssel, Kevin Fadeur, Marjorie Tappy, Luc Paquot, Nicolas Tran, Christel |
| description | 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.
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, |
| doi_str_mv | 10.1016/j.clnu.2021.01.026 |
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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.
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).
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.
•Hereditary fructose intolerance (HFI) is an inborn error of fructose metabolism.•Heterozygous carriers for HFI are considered as healthy carriers.•We assessed the impact of oral fructose on metabolic parameters in carriers for HFI.•Postprandial uric acid and insulin concentrations increased in carriers for HFI only.</description><identifier>ISSN: 0261-5614</identifier><identifier>ISSN: 1532-1983</identifier><identifier>EISSN: 1532-1983</identifier><identifier>DOI: 10.1016/j.clnu.2021.01.026</identifier><identifier>PMID: 33551217</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Adult ; Blood Glucose ; Blood Glucose - metabolism ; Critical Care and Intensive Care Medicine ; Cross-Over Studies ; Diet, Carbohydrate Loading ; Diet, Carbohydrate Loading - adverse effects ; Diet, Carbohydrate Loading - methods ; Endocrinologie, métabolisme & nutrition ; Endocrinology, metabolism & nutrition ; Fasting ; Fasting - blood ; Female ; Fructose ; Fructose - administration & dosage ; Fructose - adverse effects ; Fructose Intolerance ; Fructose Intolerance - blood ; Fructose Intolerance - genetics ; Fructose-Bisphosphate Aldolase ; Fructose-Bisphosphate Aldolase - genetics ; Glucose ; Glucose - administration & dosage ; Glucose - adverse effects ; Healthy carriers ; Hereditary fructose intolerance ; Heterozygote ; Human health sciences ; Humans ; Hyperuricemia ; Hyperuricemia - etiology ; Hyperuricemia - genetics ; Insulin ; Insulin - blood ; Insulin Resistance ; Insulin Resistance - genetics ; Liver ; Liver - metabolism ; Male ; Meals ; Meals - physiology ; Metabolic Syndrome ; Metabolic Syndrome - blood ; Metabolic Syndrome - genetics ; Nutrition and Dietetics ; Postprandial Period ; Sciences de la santé humaine ; Uric acid ; Uric Acid - blood</subject><ispartof>Clinical nutrition (Edinburgh, Scotland), 2021-06, Vol.40 (6), p.4246-4254</ispartof><rights>2021 The Author(s)</rights><rights>Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c444t-c0df3b75feab50327bd63e3b828068bd24b3e046688cc49330402281a227fb4d3</citedby><cites>FETCH-LOGICAL-c444t-c0df3b75feab50327bd63e3b828068bd24b3e046688cc49330402281a227fb4d3</cites><orcidid>0000-0001-8469-4692 ; 0000-0003-4158-536X ; 0000-0002-7086-6630</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.clnu.2021.01.026$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,315,781,785,886,3551,27926,27927,45997</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33551217$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Debray, François-Guillaume</creatorcontrib><creatorcontrib>Seyssel, Kevin</creatorcontrib><creatorcontrib>Fadeur, Marjorie</creatorcontrib><creatorcontrib>Tappy, Luc</creatorcontrib><creatorcontrib>Paquot, Nicolas</creatorcontrib><creatorcontrib>Tran, Christel</creatorcontrib><title>Effect of a high fructose diet on metabolic parameters in carriers for hereditary fructose intolerance</title><title>Clinical nutrition (Edinburgh, Scotland)</title><addtitle>Clin Nutr</addtitle><description>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.
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.
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).
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.
•Hereditary fructose intolerance (HFI) is an inborn error of fructose metabolism.•Heterozygous carriers for HFI are considered as healthy carriers.•We assessed the impact of oral fructose on metabolic parameters in carriers for HFI.•Postprandial uric acid and insulin concentrations increased in carriers for HFI only.</description><subject>Adult</subject><subject>Blood Glucose</subject><subject>Blood Glucose - metabolism</subject><subject>Critical Care and Intensive Care Medicine</subject><subject>Cross-Over Studies</subject><subject>Diet, Carbohydrate Loading</subject><subject>Diet, Carbohydrate Loading - adverse effects</subject><subject>Diet, Carbohydrate Loading - methods</subject><subject>Endocrinologie, métabolisme & nutrition</subject><subject>Endocrinology, metabolism & nutrition</subject><subject>Fasting</subject><subject>Fasting - blood</subject><subject>Female</subject><subject>Fructose</subject><subject>Fructose - administration & dosage</subject><subject>Fructose - adverse effects</subject><subject>Fructose Intolerance</subject><subject>Fructose Intolerance - blood</subject><subject>Fructose Intolerance - genetics</subject><subject>Fructose-Bisphosphate Aldolase</subject><subject>Fructose-Bisphosphate Aldolase - genetics</subject><subject>Glucose</subject><subject>Glucose - administration & dosage</subject><subject>Glucose - adverse effects</subject><subject>Healthy carriers</subject><subject>Hereditary fructose intolerance</subject><subject>Heterozygote</subject><subject>Human health sciences</subject><subject>Humans</subject><subject>Hyperuricemia</subject><subject>Hyperuricemia - etiology</subject><subject>Hyperuricemia - genetics</subject><subject>Insulin</subject><subject>Insulin - blood</subject><subject>Insulin Resistance</subject><subject>Insulin Resistance - genetics</subject><subject>Liver</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Meals</subject><subject>Meals - physiology</subject><subject>Metabolic Syndrome</subject><subject>Metabolic Syndrome - blood</subject><subject>Metabolic Syndrome - genetics</subject><subject>Nutrition and Dietetics</subject><subject>Postprandial Period</subject><subject>Sciences de la santé humaine</subject><subject>Uric acid</subject><subject>Uric Acid - blood</subject><issn>0261-5614</issn><issn>1532-1983</issn><issn>1532-1983</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UU1r3DAQFaWh2W76B3ooOvbirTSSZS30UkL6AYFekrOQ5NGuFq-1lexA_31knLa3wsCMhveemPcIec_ZjjOuPp12fhjnHTDgO1YL1Cuy4a2Ahu-1eE02dcObVnF5Td6WcmKMtaLTb8i1EG3LgXcbEu5CQD_RFKilx3g40pBnP6WCtI9Y9yM942RdGqKnF5ttfWEuNI7U25zjMoeU6REz9nGy-fc_gThOacBsR4835CrYoeC7l74lj1_vHm6_N_c_v_24_XLfeCnl1HjWB-G6NqB1LRPQuV4JFE6DZkq7HqQTyKRSWnsv90IwyQA0twBdcLIXWyJW3SHiAU3KLponMMnGdZ6Hg7HeODQAShvYK6l0ZX1cWZecfs1YJnOOxeMw2BHTXAxI3UnBlw-3BFaoz6mUjMFccjzXsw1nZknFnMySillSMawWqEr68KI_uzP2fyl_YqiAzysAqzdP1VRTfMTqWx9zTcf0Kf5P_xkRFJ41</recordid><startdate>20210601</startdate><enddate>20210601</enddate><creator>Debray, François-Guillaume</creator><creator>Seyssel, Kevin</creator><creator>Fadeur, Marjorie</creator><creator>Tappy, Luc</creator><creator>Paquot, Nicolas</creator><creator>Tran, Christel</creator><general>Elsevier Ltd</general><general>Churchill Livingstone</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>Q33</scope><orcidid>https://orcid.org/0000-0001-8469-4692</orcidid><orcidid>https://orcid.org/0000-0003-4158-536X</orcidid><orcidid>https://orcid.org/0000-0002-7086-6630</orcidid></search><sort><creationdate>20210601</creationdate><title>Effect of a high fructose diet on metabolic parameters in carriers for hereditary fructose intolerance</title><author>Debray, François-Guillaume ; Seyssel, Kevin ; Fadeur, Marjorie ; Tappy, Luc ; Paquot, Nicolas ; Tran, Christel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-c0df3b75feab50327bd63e3b828068bd24b3e046688cc49330402281a227fb4d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adult</topic><topic>Blood Glucose</topic><topic>Blood Glucose - metabolism</topic><topic>Critical Care and Intensive Care Medicine</topic><topic>Cross-Over Studies</topic><topic>Diet, Carbohydrate Loading</topic><topic>Diet, Carbohydrate Loading - adverse effects</topic><topic>Diet, Carbohydrate Loading - methods</topic><topic>Endocrinologie, métabolisme & nutrition</topic><topic>Endocrinology, metabolism & nutrition</topic><topic>Fasting</topic><topic>Fasting - blood</topic><topic>Female</topic><topic>Fructose</topic><topic>Fructose - administration & dosage</topic><topic>Fructose - adverse effects</topic><topic>Fructose Intolerance</topic><topic>Fructose Intolerance - blood</topic><topic>Fructose Intolerance - genetics</topic><topic>Fructose-Bisphosphate Aldolase</topic><topic>Fructose-Bisphosphate Aldolase - genetics</topic><topic>Glucose</topic><topic>Glucose - administration & dosage</topic><topic>Glucose - adverse effects</topic><topic>Healthy carriers</topic><topic>Hereditary fructose intolerance</topic><topic>Heterozygote</topic><topic>Human health sciences</topic><topic>Humans</topic><topic>Hyperuricemia</topic><topic>Hyperuricemia - etiology</topic><topic>Hyperuricemia - genetics</topic><topic>Insulin</topic><topic>Insulin - blood</topic><topic>Insulin Resistance</topic><topic>Insulin Resistance - genetics</topic><topic>Liver</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>Meals</topic><topic>Meals - physiology</topic><topic>Metabolic Syndrome</topic><topic>Metabolic Syndrome - blood</topic><topic>Metabolic Syndrome - genetics</topic><topic>Nutrition and Dietetics</topic><topic>Postprandial Period</topic><topic>Sciences de la santé humaine</topic><topic>Uric acid</topic><topic>Uric Acid - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Debray, François-Guillaume</creatorcontrib><creatorcontrib>Seyssel, Kevin</creatorcontrib><creatorcontrib>Fadeur, Marjorie</creatorcontrib><creatorcontrib>Tappy, Luc</creatorcontrib><creatorcontrib>Paquot, Nicolas</creatorcontrib><creatorcontrib>Tran, Christel</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Université de Liège - Open Repository and Bibliography (ORBI)</collection><jtitle>Clinical nutrition (Edinburgh, Scotland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Debray, François-Guillaume</au><au>Seyssel, Kevin</au><au>Fadeur, Marjorie</au><au>Tappy, Luc</au><au>Paquot, Nicolas</au><au>Tran, Christel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of a high fructose diet on metabolic parameters in carriers for hereditary fructose intolerance</atitle><jtitle>Clinical nutrition (Edinburgh, Scotland)</jtitle><addtitle>Clin Nutr</addtitle><date>2021-06-01</date><risdate>2021</risdate><volume>40</volume><issue>6</issue><spage>4246</spage><epage>4254</epage><pages>4246-4254</pages><issn>0261-5614</issn><issn>1532-1983</issn><eissn>1532-1983</eissn><abstract>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.
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.
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).
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.
•Hereditary fructose intolerance (HFI) is an inborn error of fructose metabolism.•Heterozygous carriers for HFI are considered as healthy carriers.•We assessed the impact of oral fructose on metabolic parameters in carriers for HFI.•Postprandial uric acid and insulin concentrations increased in carriers for HFI only.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>33551217</pmid><doi>10.1016/j.clnu.2021.01.026</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-8469-4692</orcidid><orcidid>https://orcid.org/0000-0003-4158-536X</orcidid><orcidid>https://orcid.org/0000-0002-7086-6630</orcidid><oa>free_for_read</oa></addata></record> |
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| language | eng |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Adult Blood Glucose Blood Glucose - metabolism Critical Care and Intensive Care Medicine Cross-Over Studies Diet, Carbohydrate Loading Diet, Carbohydrate Loading - adverse effects Diet, Carbohydrate Loading - methods Endocrinologie, métabolisme & nutrition Endocrinology, metabolism & nutrition Fasting Fasting - blood Female Fructose Fructose - administration & dosage Fructose - adverse effects Fructose Intolerance Fructose Intolerance - blood Fructose Intolerance - genetics Fructose-Bisphosphate Aldolase Fructose-Bisphosphate Aldolase - genetics Glucose Glucose - administration & dosage Glucose - adverse effects Healthy carriers Hereditary fructose intolerance Heterozygote Human health sciences Humans Hyperuricemia Hyperuricemia - etiology Hyperuricemia - genetics Insulin Insulin - blood Insulin Resistance Insulin Resistance - genetics Liver Liver - metabolism Male Meals Meals - physiology Metabolic Syndrome Metabolic Syndrome - blood Metabolic Syndrome - genetics Nutrition and Dietetics Postprandial Period Sciences de la santé humaine Uric acid Uric Acid - blood |
| title | Effect of a high fructose diet on metabolic parameters in carriers for hereditary fructose intolerance |
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