Chronic fructose intake does not induce liver steatosis and inflammation in female Sprague-Dawley rats, but causes hypertriglyceridemia related to decreased VLDL receptor expression

Purpose: Sugar-sweetened beverage intake is a risk factor for insulin resistance, dyslipidemia, fatty liver, and steatohepatitis (NASH). Sub-chronic supplementation of liquid fructose, but not glucose, in female rats increases liver and plasma triglycerides without inflammation. We hypothesized that...

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Autores: Sangüesa Puigventós, Gemma, Montañés, José Carlos, Baena Muñoz, Miguel, Sánchez, Rosa María, Roglans i Ribas, Núria, Alegret i Jordà, Marta, Laguna Egea, Juan Carlos
Tipo de recurso: artículo
Estado:Versión aceptada para publicación
Fecha de publicación:2019
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/205843
Acceso en línea:https://hdl.handle.net/2445/205843
Access Level:acceso abierto
Palabra clave:Fructosa
Malalties del fetge
Àcids grassos
Fructose
Liver diseases
Fatty acids
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spelling Chronic fructose intake does not induce liver steatosis and inflammation in female Sprague-Dawley rats, but causes hypertriglyceridemia related to decreased VLDL receptor expressionSangüesa Puigventós, GemmaMontañés, José CarlosBaena Muñoz, MiguelSánchez, Rosa MaríaRoglans i Ribas, NúriaAlegret i Jordà, MartaLaguna Egea, Juan CarlosFructosaMalalties del fetgeÀcids grassosFructoseLiver diseasesFatty acidsPurpose: Sugar-sweetened beverage intake is a risk factor for insulin resistance, dyslipidemia, fatty liver, and steatohepatitis (NASH). Sub-chronic supplementation of liquid fructose, but not glucose, in female rats increases liver and plasma triglycerides without inflammation. We hypothesized that chronic supplementation of fructose would cause NASH and liver insulin resistance. Methods: We supplemented female Sprague-Dawley rats with water or either fructose or glucose 10% w/v solutions under isocaloric conditions for 7 months. At the end, plasma analytes, insulin, and adiponectin were determined, as well as liver triglyceride content and the expression of key genes controlling inflammation, fatty acid synthesis and oxidation, endoplasmic reticulum stress, and plasma VLDL clearance, by biochemical and histological methods. Results: Although sugar-supplemented rats increased their energy intake by 50-60%, we found no manifestation of liver steatosis, fibrosis or necrosis, unchanged plasma or tissue markers of inflammation or fibrosis, and reduced liver expression of gluconeogenic enzymes, despite both sugars increased fatty acid synthesis, mTORC1, and IRE1 activity, while decreasing fatty acid oxidation and PPARα activity. Only fructose-supplemented rats were hypertriglyceridemic, showing a reduced expression of VLDL receptor and lipoprotein lipase in skeletal muscle and vWAT. Glucose-supplemented rats showed increased adiponectinemia, which would explain the different metabolic outcomes of the two sugars. Conclusions: Chronic liquid simple sugar supplementation, as the sole risk factor, is not enough for female rats to develop NASH and increased liver gluconeogenesis. Nevertheless, under isocaloric conditions, only fructose induced hypertriglyceridemia, thus confirming that also the type of nutrient matters in the development of metabolic diseases. Keywords: Endoplasmic reticulum stress; Fatty acid metabolism; Glucose; NAFLD; UPR response.Springer Verlag2024202420192024info:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersion15 p.application/pdfapplication/pdfhttps://hdl.handle.net/2445/205843Articles publicats en revistes (Farmacologia, Toxicologia i Química Terapèutica)reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)InglésVersió postprint del document publicat a: https://doi.org/10.1007/s00394-018-1654-9European Journal of Nutrition, 2019, vol. 58, num.3, p. 1283-1297https://doi.org/10.1007/s00394-018-1654-9(c) Springer Verlag, 2019info:eu-repo/semantics/openAccessoai:recercat.cat:2445/2058432026-05-29T05:05:01Z
dc.title.none.fl_str_mv Chronic fructose intake does not induce liver steatosis and inflammation in female Sprague-Dawley rats, but causes hypertriglyceridemia related to decreased VLDL receptor expression
title Chronic fructose intake does not induce liver steatosis and inflammation in female Sprague-Dawley rats, but causes hypertriglyceridemia related to decreased VLDL receptor expression
spellingShingle Chronic fructose intake does not induce liver steatosis and inflammation in female Sprague-Dawley rats, but causes hypertriglyceridemia related to decreased VLDL receptor expression
Sangüesa Puigventós, Gemma
Fructosa
Malalties del fetge
Àcids grassos
Fructose
Liver diseases
Fatty acids
title_short Chronic fructose intake does not induce liver steatosis and inflammation in female Sprague-Dawley rats, but causes hypertriglyceridemia related to decreased VLDL receptor expression
title_full Chronic fructose intake does not induce liver steatosis and inflammation in female Sprague-Dawley rats, but causes hypertriglyceridemia related to decreased VLDL receptor expression
title_fullStr Chronic fructose intake does not induce liver steatosis and inflammation in female Sprague-Dawley rats, but causes hypertriglyceridemia related to decreased VLDL receptor expression
title_full_unstemmed Chronic fructose intake does not induce liver steatosis and inflammation in female Sprague-Dawley rats, but causes hypertriglyceridemia related to decreased VLDL receptor expression
title_sort Chronic fructose intake does not induce liver steatosis and inflammation in female Sprague-Dawley rats, but causes hypertriglyceridemia related to decreased VLDL receptor expression
dc.creator.none.fl_str_mv Sangüesa Puigventós, Gemma
Montañés, José Carlos
Baena Muñoz, Miguel
Sánchez, Rosa María
Roglans i Ribas, Núria
Alegret i Jordà, Marta
Laguna Egea, Juan Carlos
author Sangüesa Puigventós, Gemma
author_facet Sangüesa Puigventós, Gemma
Montañés, José Carlos
Baena Muñoz, Miguel
Sánchez, Rosa María
Roglans i Ribas, Núria
Alegret i Jordà, Marta
Laguna Egea, Juan Carlos
author_role author
author2 Montañés, José Carlos
Baena Muñoz, Miguel
Sánchez, Rosa María
Roglans i Ribas, Núria
Alegret i Jordà, Marta
Laguna Egea, Juan Carlos
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv Fructosa
Malalties del fetge
Àcids grassos
Fructose
Liver diseases
Fatty acids
topic Fructosa
Malalties del fetge
Àcids grassos
Fructose
Liver diseases
Fatty acids
description Purpose: Sugar-sweetened beverage intake is a risk factor for insulin resistance, dyslipidemia, fatty liver, and steatohepatitis (NASH). Sub-chronic supplementation of liquid fructose, but not glucose, in female rats increases liver and plasma triglycerides without inflammation. We hypothesized that chronic supplementation of fructose would cause NASH and liver insulin resistance. Methods: We supplemented female Sprague-Dawley rats with water or either fructose or glucose 10% w/v solutions under isocaloric conditions for 7 months. At the end, plasma analytes, insulin, and adiponectin were determined, as well as liver triglyceride content and the expression of key genes controlling inflammation, fatty acid synthesis and oxidation, endoplasmic reticulum stress, and plasma VLDL clearance, by biochemical and histological methods. Results: Although sugar-supplemented rats increased their energy intake by 50-60%, we found no manifestation of liver steatosis, fibrosis or necrosis, unchanged plasma or tissue markers of inflammation or fibrosis, and reduced liver expression of gluconeogenic enzymes, despite both sugars increased fatty acid synthesis, mTORC1, and IRE1 activity, while decreasing fatty acid oxidation and PPARα activity. Only fructose-supplemented rats were hypertriglyceridemic, showing a reduced expression of VLDL receptor and lipoprotein lipase in skeletal muscle and vWAT. Glucose-supplemented rats showed increased adiponectinemia, which would explain the different metabolic outcomes of the two sugars. Conclusions: Chronic liquid simple sugar supplementation, as the sole risk factor, is not enough for female rats to develop NASH and increased liver gluconeogenesis. Nevertheless, under isocaloric conditions, only fructose induced hypertriglyceridemia, thus confirming that also the type of nutrient matters in the development of metabolic diseases. Keywords: Endoplasmic reticulum stress; Fatty acid metabolism; Glucose; NAFLD; UPR response.
publishDate 2019
dc.date.none.fl_str_mv 2019
2024
2024
2024
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/acceptedVersion
format article
status_str acceptedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/205843
url https://hdl.handle.net/2445/205843
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Versió postprint del document publicat a: https://doi.org/10.1007/s00394-018-1654-9
European Journal of Nutrition, 2019, vol. 58, num.3, p. 1283-1297
https://doi.org/10.1007/s00394-018-1654-9
dc.rights.none.fl_str_mv (c) Springer Verlag, 2019
info:eu-repo/semantics/openAccess
rights_invalid_str_mv (c) Springer Verlag, 2019
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 15 p.
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Springer Verlag
publisher.none.fl_str_mv Springer Verlag
dc.source.none.fl_str_mv Articles publicats en revistes (Farmacologia, Toxicologia i Química Terapèutica)
reponame:Recercat. Dipósit de la Recerca de Catalunya
instname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
instname_str Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
reponame_str Recercat. Dipósit de la Recerca de Catalunya
collection Recercat. Dipósit de la Recerca de Catalunya
repository.name.fl_str_mv
repository.mail.fl_str_mv
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