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Evidence for Toxic Advanced Glycation End-Products Generated in the Normal Rat Liver

Glucose/fructose in beverages/foods containing high-fructose corn syrup (HFCS) are metabolized to glyceraldehyde (GA) in the liver. We previously reported that GA-derived advanced glycation end-products (toxic AGEs, TAGE) are generated and may induce the onset/progression of non-alcoholic fatty live...

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Autores principales: Takata, Takanobu, Sakasai-Sakai, Akiko, Takino, Jun-ichi, Takeuchi, Masayoshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6683103/
https://www.ncbi.nlm.nih.gov/pubmed/31315223
http://dx.doi.org/10.3390/nu11071612
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author Takata, Takanobu
Sakasai-Sakai, Akiko
Takino, Jun-ichi
Takeuchi, Masayoshi
author_facet Takata, Takanobu
Sakasai-Sakai, Akiko
Takino, Jun-ichi
Takeuchi, Masayoshi
author_sort Takata, Takanobu
collection PubMed
description Glucose/fructose in beverages/foods containing high-fructose corn syrup (HFCS) are metabolized to glyceraldehyde (GA) in the liver. We previously reported that GA-derived advanced glycation end-products (toxic AGEs, TAGE) are generated and may induce the onset/progression of non-alcoholic fatty liver disease (NAFLD). We revealed that the generation of TAGE in the liver and serum TAGE levels were higher in NAFLD patients than in healthy humans. Although we propose the intracellular generation of TAGE in the normal liver, there is currently no evidence to support this, and the levels of TAGE produced have not yet been measured. In the present study, male Wister/ST rats that drank normal water or 10% HFCS 55 (HFCS beverage) were maintained for 13 weeks, and serum TAGE levels and intracellular TAGE levels in the liver were analyzed. Rats in the HFCS group drank 127.4 mL of the HFCS beverage each day. Serum TAGE levels and intracellular TAGE levels in the liver both increased in the HFCS group. A positive correlation was observed between intracellular TAGE levels in the liver and serum TAGE levels. On the other hand, in male Wister/ST rats that drank Lactobacillus beverage for 12 weeks—a commercial drink that contains glucose, fructose, and sucrose— no increases were observed in intracellular TAGE or serum TAGE levels. Intracellular TAGE were generated in the normal rat liver, and their production was promoted by HFCS, which may increase the risk of NAFLD.
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spelling pubmed-66831032019-08-09 Evidence for Toxic Advanced Glycation End-Products Generated in the Normal Rat Liver Takata, Takanobu Sakasai-Sakai, Akiko Takino, Jun-ichi Takeuchi, Masayoshi Nutrients Article Glucose/fructose in beverages/foods containing high-fructose corn syrup (HFCS) are metabolized to glyceraldehyde (GA) in the liver. We previously reported that GA-derived advanced glycation end-products (toxic AGEs, TAGE) are generated and may induce the onset/progression of non-alcoholic fatty liver disease (NAFLD). We revealed that the generation of TAGE in the liver and serum TAGE levels were higher in NAFLD patients than in healthy humans. Although we propose the intracellular generation of TAGE in the normal liver, there is currently no evidence to support this, and the levels of TAGE produced have not yet been measured. In the present study, male Wister/ST rats that drank normal water or 10% HFCS 55 (HFCS beverage) were maintained for 13 weeks, and serum TAGE levels and intracellular TAGE levels in the liver were analyzed. Rats in the HFCS group drank 127.4 mL of the HFCS beverage each day. Serum TAGE levels and intracellular TAGE levels in the liver both increased in the HFCS group. A positive correlation was observed between intracellular TAGE levels in the liver and serum TAGE levels. On the other hand, in male Wister/ST rats that drank Lactobacillus beverage for 12 weeks—a commercial drink that contains glucose, fructose, and sucrose— no increases were observed in intracellular TAGE or serum TAGE levels. Intracellular TAGE were generated in the normal rat liver, and their production was promoted by HFCS, which may increase the risk of NAFLD. MDPI 2019-07-16 /pmc/articles/PMC6683103/ /pubmed/31315223 http://dx.doi.org/10.3390/nu11071612 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Takata, Takanobu
Sakasai-Sakai, Akiko
Takino, Jun-ichi
Takeuchi, Masayoshi
Evidence for Toxic Advanced Glycation End-Products Generated in the Normal Rat Liver
title Evidence for Toxic Advanced Glycation End-Products Generated in the Normal Rat Liver
title_full Evidence for Toxic Advanced Glycation End-Products Generated in the Normal Rat Liver
title_fullStr Evidence for Toxic Advanced Glycation End-Products Generated in the Normal Rat Liver
title_full_unstemmed Evidence for Toxic Advanced Glycation End-Products Generated in the Normal Rat Liver
title_short Evidence for Toxic Advanced Glycation End-Products Generated in the Normal Rat Liver
title_sort evidence for toxic advanced glycation end-products generated in the normal rat liver
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6683103/
https://www.ncbi.nlm.nih.gov/pubmed/31315223
http://dx.doi.org/10.3390/nu11071612
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