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High fructose diet suppresses exercise-induced increase in AQP7 expression in the in vivo rat heart
OBJECTIVE: Cardiac uptake of fructose is thought to be mediated by glucose transporter 5 (GLUT5), whereas the uptake of glycerol is facilitated by aquaporin 7 (AQP7). We aimed to investigate the effect of a high-fructose diet (HFD) on GLUT5 and AQP7 levels in the rat heart subjected to exercise. MET...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Kare Publishing
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5324910/ https://www.ncbi.nlm.nih.gov/pubmed/27182614 http://dx.doi.org/10.14744/AnatolJCardiol.2016.6958 |
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author | Karaca, Aziz Palabıyık, Orkide Taştekin, Ebru Turan, Fatma Nesrin Vardar, Selma Arzu |
author_facet | Karaca, Aziz Palabıyık, Orkide Taştekin, Ebru Turan, Fatma Nesrin Vardar, Selma Arzu |
author_sort | Karaca, Aziz |
collection | PubMed |
description | OBJECTIVE: Cardiac uptake of fructose is thought to be mediated by glucose transporter 5 (GLUT5), whereas the uptake of glycerol is facilitated by aquaporin 7 (AQP7). We aimed to investigate the effect of a high-fructose diet (HFD) on GLUT5 and AQP7 levels in the rat heart subjected to exercise. METHODS: Male Sprague–Dawley rats were allocated to control (C; n=11), exercise (E; n=10), HFD (n=12), and HFD plus exercise (HFD-E; n=12) groups. HFD was started 28 days before euthanasia. From day 24 to 27, rats were subjected to moderate exercise, followed by vigorous exercise on day 28 (groups E and HFD-E). Cardiac GLUT5 and AQP7 mRNA levels were determined using RT-PCR. The protein contents of GLUT5 and AQP7 were immunohistochemically assessed. Paired-t, ANOVA with Bonferroni, Kruskal–Wallis, and Bonferroni-corrected Mann–Whitney U tests were used for statistical analysis. RESULTS: GLUT5 mRNA expression and protein content did not differ between the groups. AQP7 mRNA levels significantly increased (4.8-fold) in group E compared with in group C (p<0.001). Compared with group C, no significant change was observed in AQP7 mRNA levels in groups HFD and HFD-E. The AQP7 staining score in group E was significantly higher than that in groups C (p<0.001), E (p<0.001), and HFD-E (p<0.001). CONCLUSION: Our study indicates that exercise enhances cardiac AQP7 mRNA expression and protein content. However, HFD prevents the exercise-induced increase in cardiac AQP7 expression. This inhibitory effect may be related to the competition between fructose and glycerol as energy substrates in the rat heart subjected to 5 days of physical exercise. (Anatol J Cardiol 2016; 16: 916-22) |
format | Online Article Text |
id | pubmed-5324910 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Kare Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-53249102017-06-28 High fructose diet suppresses exercise-induced increase in AQP7 expression in the in vivo rat heart Karaca, Aziz Palabıyık, Orkide Taştekin, Ebru Turan, Fatma Nesrin Vardar, Selma Arzu Anatol J Cardiol Original Investigation OBJECTIVE: Cardiac uptake of fructose is thought to be mediated by glucose transporter 5 (GLUT5), whereas the uptake of glycerol is facilitated by aquaporin 7 (AQP7). We aimed to investigate the effect of a high-fructose diet (HFD) on GLUT5 and AQP7 levels in the rat heart subjected to exercise. METHODS: Male Sprague–Dawley rats were allocated to control (C; n=11), exercise (E; n=10), HFD (n=12), and HFD plus exercise (HFD-E; n=12) groups. HFD was started 28 days before euthanasia. From day 24 to 27, rats were subjected to moderate exercise, followed by vigorous exercise on day 28 (groups E and HFD-E). Cardiac GLUT5 and AQP7 mRNA levels were determined using RT-PCR. The protein contents of GLUT5 and AQP7 were immunohistochemically assessed. Paired-t, ANOVA with Bonferroni, Kruskal–Wallis, and Bonferroni-corrected Mann–Whitney U tests were used for statistical analysis. RESULTS: GLUT5 mRNA expression and protein content did not differ between the groups. AQP7 mRNA levels significantly increased (4.8-fold) in group E compared with in group C (p<0.001). Compared with group C, no significant change was observed in AQP7 mRNA levels in groups HFD and HFD-E. The AQP7 staining score in group E was significantly higher than that in groups C (p<0.001), E (p<0.001), and HFD-E (p<0.001). CONCLUSION: Our study indicates that exercise enhances cardiac AQP7 mRNA expression and protein content. However, HFD prevents the exercise-induced increase in cardiac AQP7 expression. This inhibitory effect may be related to the competition between fructose and glycerol as energy substrates in the rat heart subjected to 5 days of physical exercise. (Anatol J Cardiol 2016; 16: 916-22) Kare Publishing 2016-12 2016-04-26 /pmc/articles/PMC5324910/ /pubmed/27182614 http://dx.doi.org/10.14744/AnatolJCardiol.2016.6958 Text en Copyright © 2016 Turkish Society of Cardiology http://creativecommons.org/licenses/by-nc-sa/4.0 This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License |
spellingShingle | Original Investigation Karaca, Aziz Palabıyık, Orkide Taştekin, Ebru Turan, Fatma Nesrin Vardar, Selma Arzu High fructose diet suppresses exercise-induced increase in AQP7 expression in the in vivo rat heart |
title | High fructose diet suppresses exercise-induced increase in AQP7 expression in the in vivo rat heart |
title_full | High fructose diet suppresses exercise-induced increase in AQP7 expression in the in vivo rat heart |
title_fullStr | High fructose diet suppresses exercise-induced increase in AQP7 expression in the in vivo rat heart |
title_full_unstemmed | High fructose diet suppresses exercise-induced increase in AQP7 expression in the in vivo rat heart |
title_short | High fructose diet suppresses exercise-induced increase in AQP7 expression in the in vivo rat heart |
title_sort | high fructose diet suppresses exercise-induced increase in aqp7 expression in the in vivo rat heart |
topic | Original Investigation |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5324910/ https://www.ncbi.nlm.nih.gov/pubmed/27182614 http://dx.doi.org/10.14744/AnatolJCardiol.2016.6958 |
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