Mechanistically different effects of fat and sugar on insulin resistance, hypertension and gut microbiota in rats

Insulin resistance (IR) and impaired glucose tolerance (IGT) are the first manifestations of diet-induced metabolic alterations leading to type-2 diabetes, while hypertension is the deadliest risk factor of cardiovascular disease. The roles of dietary fat and fructose in the development of IR, IGT a...

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Authors: Ramos Romero, Sara, Hereu, Mercè, Atienza, Lidia, Casas, Josefina, Jáuregui, Olga, Amézqueta, Susana, Dasilva, Gabriel, Medina, Isabel, Nogués, Maria Rosa, Romeu Ferran, Marta, Torres, Josep Lluís
Format: article
Status:Versión aceptada para publicación
Publication Date:2018
Country:España
Institution:Universidad de Barcelona
Repository:Dipòsit Digital de la UB
OAI Identifier:oai:diposit.ub.edu:2445/162316
Online Access:https://hdl.handle.net/2445/162316
Access Level:Open access
Keyword:Microbiota
Diabetis
Hipertensió
Obesitat
Diabetes
Hypertension
Obesity
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spelling Mechanistically different effects of fat and sugar on insulin resistance, hypertension and gut microbiota in ratsRamos Romero, SaraHereu, MercèAtienza, LidiaCasas, JosefinaJáuregui, OlgaAmézqueta, SusanaDasilva, GabrielMedina, IsabelNogués, Maria RosaRomeu Ferran, MartaTorres, Josep LluísMicrobiotaDiabetisHipertensióObesitatMicrobiotaDiabetesHypertensionObesityInsulin resistance (IR) and impaired glucose tolerance (IGT) are the first manifestations of diet-induced metabolic alterations leading to type-2 diabetes, while hypertension is the deadliest risk factor of cardiovascular disease. The roles of dietary fat and fructose in the development of IR, IGT and hypertension are controversial. We tested the long-term effects of an excess of fat or sucrose (fructose/glucose) on healthy male Wistar Kyoto (WKY) rats. Fat affects IR and IGT earlier than fructose through low-grade systemic inflammation evidenced by liver inflammatory infiltration, increased levels of plasma interleukin-6, prostaglandin E2 and reduced levels of protective short-chain fatty acids without triggering hypertension. Increased populations of gut Enterobacteriales and Escherichia coli may contribute to systemic inflammation through the generation of lipopolysaccharides. Unlike fat, fructose induces increased levels of diacylglycerols (lipid mediators of IR) in the liver, urine F2-isoprostanes (markers of systemic oxidative stress) and uric acid, and triggers hypertension. Elevated populations of Enterobacteriales and E. coli were only detected in rats given an excess of fructose at the end of the study. Dietary fat and fructose trigger IR and IGT in clearly differentiated ways in WKY rats: early low-grade inflammation and late direct lipid toxicity, respectively; gut microbiota plays a role mainly in fat-induced IR; and hypertension is independent of inflammation55 mediated IR. The results provide evidence which suggests that the combination of fat and sugar is potentially more harmful than fat or sugar alone when taken in excess.American Physiological Society2018info:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersionapplication/pdfhttps://hdl.handle.net/2445/162316Articles publicats en revistes (Enginyeria Química i Química Analítica)reponame:Dipòsit Digital de la UBinstname:Universidad de BarcelonaInglésVersió postprint del document publicat a: https://doi.org/10.1152/ajpendo.00323.2017American Journal of Physiology, 2018, vol. 314, num. 6, p. E552-E563https://doi.org/10.1152/ajpendo.00323.2017(c) American Physiological Society, 2018info:eu-repo/semantics/openAccessoai:diposit.ub.edu:2445/1623162026-05-27T06:46:51Z
dc.title.none.fl_str_mv Mechanistically different effects of fat and sugar on insulin resistance, hypertension and gut microbiota in rats
title Mechanistically different effects of fat and sugar on insulin resistance, hypertension and gut microbiota in rats
spellingShingle Mechanistically different effects of fat and sugar on insulin resistance, hypertension and gut microbiota in rats
Ramos Romero, Sara
Microbiota
Diabetis
Hipertensió
Obesitat
Microbiota
Diabetes
Hypertension
Obesity
title_short Mechanistically different effects of fat and sugar on insulin resistance, hypertension and gut microbiota in rats
title_full Mechanistically different effects of fat and sugar on insulin resistance, hypertension and gut microbiota in rats
title_fullStr Mechanistically different effects of fat and sugar on insulin resistance, hypertension and gut microbiota in rats
title_full_unstemmed Mechanistically different effects of fat and sugar on insulin resistance, hypertension and gut microbiota in rats
title_sort Mechanistically different effects of fat and sugar on insulin resistance, hypertension and gut microbiota in rats
dc.creator.none.fl_str_mv Ramos Romero, Sara
Hereu, Mercè
Atienza, Lidia
Casas, Josefina
Jáuregui, Olga
Amézqueta, Susana
Dasilva, Gabriel
Medina, Isabel
Nogués, Maria Rosa
Romeu Ferran, Marta
Torres, Josep Lluís
author Ramos Romero, Sara
author_facet Ramos Romero, Sara
Hereu, Mercè
Atienza, Lidia
Casas, Josefina
Jáuregui, Olga
Amézqueta, Susana
Dasilva, Gabriel
Medina, Isabel
Nogués, Maria Rosa
Romeu Ferran, Marta
Torres, Josep Lluís
author_role author
author2 Hereu, Mercè
Atienza, Lidia
Casas, Josefina
Jáuregui, Olga
Amézqueta, Susana
Dasilva, Gabriel
Medina, Isabel
Nogués, Maria Rosa
Romeu Ferran, Marta
Torres, Josep Lluís
author2_role author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Microbiota
Diabetis
Hipertensió
Obesitat
Microbiota
Diabetes
Hypertension
Obesity
topic Microbiota
Diabetis
Hipertensió
Obesitat
Microbiota
Diabetes
Hypertension
Obesity
description Insulin resistance (IR) and impaired glucose tolerance (IGT) are the first manifestations of diet-induced metabolic alterations leading to type-2 diabetes, while hypertension is the deadliest risk factor of cardiovascular disease. The roles of dietary fat and fructose in the development of IR, IGT and hypertension are controversial. We tested the long-term effects of an excess of fat or sucrose (fructose/glucose) on healthy male Wistar Kyoto (WKY) rats. Fat affects IR and IGT earlier than fructose through low-grade systemic inflammation evidenced by liver inflammatory infiltration, increased levels of plasma interleukin-6, prostaglandin E2 and reduced levels of protective short-chain fatty acids without triggering hypertension. Increased populations of gut Enterobacteriales and Escherichia coli may contribute to systemic inflammation through the generation of lipopolysaccharides. Unlike fat, fructose induces increased levels of diacylglycerols (lipid mediators of IR) in the liver, urine F2-isoprostanes (markers of systemic oxidative stress) and uric acid, and triggers hypertension. Elevated populations of Enterobacteriales and E. coli were only detected in rats given an excess of fructose at the end of the study. Dietary fat and fructose trigger IR and IGT in clearly differentiated ways in WKY rats: early low-grade inflammation and late direct lipid toxicity, respectively; gut microbiota plays a role mainly in fat-induced IR; and hypertension is independent of inflammation55 mediated IR. The results provide evidence which suggests that the combination of fat and sugar is potentially more harmful than fat or sugar alone when taken in excess.
publishDate 2018
dc.date.none.fl_str_mv 2018
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/2445/162316
url https://hdl.handle.net/2445/162316
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/10.1152/ajpendo.00323.2017
American Journal of Physiology, 2018, vol. 314, num. 6, p. E552-E563
https://doi.org/10.1152/ajpendo.00323.2017
dc.rights.none.fl_str_mv (c) American Physiological Society, 2018
info:eu-repo/semantics/openAccess
rights_invalid_str_mv (c) American Physiological Society, 2018
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv American Physiological Society
publisher.none.fl_str_mv American Physiological Society
dc.source.none.fl_str_mv Articles publicats en revistes (Enginyeria Química i Química Analítica)
reponame:Dipòsit Digital de la UB
instname:Universidad de Barcelona
instname_str Universidad de Barcelona
reponame_str Dipòsit Digital de la UB
collection Dipòsit Digital de la UB
repository.name.fl_str_mv
repository.mail.fl_str_mv
_version_ 1869403149288079360
score 15,301603

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