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Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome
Carbohydrates with high glycemic index are proposed to promote the development of obesity, insulin resistance and fatty liver, but the mechanism by which this occurs remains unknown. High serum glucose concentrations glucose are known to induce the polyol pathway and increase fructose generation in...
Autores principales: | , , , , , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3833672/ https://www.ncbi.nlm.nih.gov/pubmed/24022321 http://dx.doi.org/10.1038/ncomms3434 |
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author | Lanaspa, Miguel A Ishimoto, Takuji Li, Nanxing Cicerchi, Christina Orlicky, David J. Ruzicky, Philip Rivard, Christopher Inaba, Shinichiro Roncal-Jimenez, Carlos A. Bales, Elise S. Diggle, Christine P. Asipu, Aruna Petrash, J. Mark Kosugi, Tomoki Maruyama, Shoichi Sanchez-Lozada, Laura G. McManaman, James L. Bonthron, David T Sautin, Yuri Y. Johnson, Richard J. |
author_facet | Lanaspa, Miguel A Ishimoto, Takuji Li, Nanxing Cicerchi, Christina Orlicky, David J. Ruzicky, Philip Rivard, Christopher Inaba, Shinichiro Roncal-Jimenez, Carlos A. Bales, Elise S. Diggle, Christine P. Asipu, Aruna Petrash, J. Mark Kosugi, Tomoki Maruyama, Shoichi Sanchez-Lozada, Laura G. McManaman, James L. Bonthron, David T Sautin, Yuri Y. Johnson, Richard J. |
author_sort | Lanaspa, Miguel A |
collection | PubMed |
description | Carbohydrates with high glycemic index are proposed to promote the development of obesity, insulin resistance and fatty liver, but the mechanism by which this occurs remains unknown. High serum glucose concentrations glucose are known to induce the polyol pathway and increase fructose generation in the liver. Here we show that this hepatic, endogenously-produced fructose causes systemic metabolic changes. We demonstrate that mice unable to metabolize fructose are protected from an increase in energy intake and body weight, visceral obesity, fatty liver, elevated insulin levels and hyperleptinemia after exposure to 10% glucose for 14 weeks. In normal mice, glucose consumption is accompanied by aldose reductase and polyol pathway activation in steatotic areas. In this regard, we show that aldose reductase deficient mice were protected against glucose-induced fatty liver. We conclude that endogenous fructose generation and metabolism in the liver represents an important mechanism whereby glucose promotes the development of metabolic syndrome. |
format | Online Article Text |
id | pubmed-3833672 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
record_format | MEDLINE/PubMed |
spelling | pubmed-38336722014-03-11 Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome Lanaspa, Miguel A Ishimoto, Takuji Li, Nanxing Cicerchi, Christina Orlicky, David J. Ruzicky, Philip Rivard, Christopher Inaba, Shinichiro Roncal-Jimenez, Carlos A. Bales, Elise S. Diggle, Christine P. Asipu, Aruna Petrash, J. Mark Kosugi, Tomoki Maruyama, Shoichi Sanchez-Lozada, Laura G. McManaman, James L. Bonthron, David T Sautin, Yuri Y. Johnson, Richard J. Nat Commun Article Carbohydrates with high glycemic index are proposed to promote the development of obesity, insulin resistance and fatty liver, but the mechanism by which this occurs remains unknown. High serum glucose concentrations glucose are known to induce the polyol pathway and increase fructose generation in the liver. Here we show that this hepatic, endogenously-produced fructose causes systemic metabolic changes. We demonstrate that mice unable to metabolize fructose are protected from an increase in energy intake and body weight, visceral obesity, fatty liver, elevated insulin levels and hyperleptinemia after exposure to 10% glucose for 14 weeks. In normal mice, glucose consumption is accompanied by aldose reductase and polyol pathway activation in steatotic areas. In this regard, we show that aldose reductase deficient mice were protected against glucose-induced fatty liver. We conclude that endogenous fructose generation and metabolism in the liver represents an important mechanism whereby glucose promotes the development of metabolic syndrome. 2013 /pmc/articles/PMC3833672/ /pubmed/24022321 http://dx.doi.org/10.1038/ncomms3434 Text en Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms |
spellingShingle | Article Lanaspa, Miguel A Ishimoto, Takuji Li, Nanxing Cicerchi, Christina Orlicky, David J. Ruzicky, Philip Rivard, Christopher Inaba, Shinichiro Roncal-Jimenez, Carlos A. Bales, Elise S. Diggle, Christine P. Asipu, Aruna Petrash, J. Mark Kosugi, Tomoki Maruyama, Shoichi Sanchez-Lozada, Laura G. McManaman, James L. Bonthron, David T Sautin, Yuri Y. Johnson, Richard J. Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome |
title | Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome |
title_full | Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome |
title_fullStr | Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome |
title_full_unstemmed | Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome |
title_short | Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome |
title_sort | endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3833672/ https://www.ncbi.nlm.nih.gov/pubmed/24022321 http://dx.doi.org/10.1038/ncomms3434 |
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