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GLUT4 content decreases along with insulin resistance and high levels of inflammatory markers in rats with metabolic syndrome

BACKGROUND: Metabolic syndrome is characterized by insulin resistance, which is closely related to GLUT4 content in insulin-sensitive tissues. Thus, we evaluated the GLUT4 expression, insulin resistance and inflammation, characteristics of the metabolic syndrome, in an experimental model. METHODS: S...

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Autores principales: Leguisamo, Natalia M, Lehnen, Alexandre M, Machado, Ubiratan F, Okamoto, Maristela M, Markoski, Melissa M, Pinto, Graziela H, Schaan, Beatriz D
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3439702/
https://www.ncbi.nlm.nih.gov/pubmed/22897936
http://dx.doi.org/10.1186/1475-2840-11-100
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author Leguisamo, Natalia M
Lehnen, Alexandre M
Machado, Ubiratan F
Okamoto, Maristela M
Markoski, Melissa M
Pinto, Graziela H
Schaan, Beatriz D
author_facet Leguisamo, Natalia M
Lehnen, Alexandre M
Machado, Ubiratan F
Okamoto, Maristela M
Markoski, Melissa M
Pinto, Graziela H
Schaan, Beatriz D
author_sort Leguisamo, Natalia M
collection PubMed
description BACKGROUND: Metabolic syndrome is characterized by insulin resistance, which is closely related to GLUT4 content in insulin-sensitive tissues. Thus, we evaluated the GLUT4 expression, insulin resistance and inflammation, characteristics of the metabolic syndrome, in an experimental model. METHODS: Spontaneously hypertensive neonate rats (18/group) were treated with monosodium glutamate (MetS) during 9 days, and compared with Wistar-Kyoto (C) and saline-treated SHR (H). Blood pressure (BP) and lipid levels, C-reactive protein (CRP), interleukin 6 (IL-6), TNF-α and adiponectin were evaluated. GLUT4 protein was analysed in the heart, white adipose tissue and gastrocnemius. Studies were performed at 3 (3-mo), 6 (6-mo) and 9 (9-mo) months of age. RESULTS: MetS rats were more insulin resistant (p<0.001, all ages) and had higher BP (3-mo: p<0.001, 6-mo: p = 0.001, 9-mo: p = 0.015) as compared to C. At 6 months, CRP, IL-6 and TNF-α were higher (p<0.001, all comparisons) in MetS rats vs H, but adiponectin was lower in MetS at 9 months (MetS: 32 ± 2, H: 42 ± 2, C: 45 ± 2 pg/mL; p<0.001). GLUT4 protein was reduced in MetS as compared to C rats at 3, 6 and 9-mo, respectively (Heart: 54%, 50% and 57%; Gastrocnemius: 37%, 56% and 50%; Adipose tissue: 69%, 61% and 69%). CONCLUSIONS: MSG-treated SHR presented all metabolic syndrome characteristics, as well as reduced GLUT4 content, which must play a key role in the impaired glycemic homeostasis of the metabolic syndrome.
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spelling pubmed-34397022012-09-13 GLUT4 content decreases along with insulin resistance and high levels of inflammatory markers in rats with metabolic syndrome Leguisamo, Natalia M Lehnen, Alexandre M Machado, Ubiratan F Okamoto, Maristela M Markoski, Melissa M Pinto, Graziela H Schaan, Beatriz D Cardiovasc Diabetol Original Investigation BACKGROUND: Metabolic syndrome is characterized by insulin resistance, which is closely related to GLUT4 content in insulin-sensitive tissues. Thus, we evaluated the GLUT4 expression, insulin resistance and inflammation, characteristics of the metabolic syndrome, in an experimental model. METHODS: Spontaneously hypertensive neonate rats (18/group) were treated with monosodium glutamate (MetS) during 9 days, and compared with Wistar-Kyoto (C) and saline-treated SHR (H). Blood pressure (BP) and lipid levels, C-reactive protein (CRP), interleukin 6 (IL-6), TNF-α and adiponectin were evaluated. GLUT4 protein was analysed in the heart, white adipose tissue and gastrocnemius. Studies were performed at 3 (3-mo), 6 (6-mo) and 9 (9-mo) months of age. RESULTS: MetS rats were more insulin resistant (p<0.001, all ages) and had higher BP (3-mo: p<0.001, 6-mo: p = 0.001, 9-mo: p = 0.015) as compared to C. At 6 months, CRP, IL-6 and TNF-α were higher (p<0.001, all comparisons) in MetS rats vs H, but adiponectin was lower in MetS at 9 months (MetS: 32 ± 2, H: 42 ± 2, C: 45 ± 2 pg/mL; p<0.001). GLUT4 protein was reduced in MetS as compared to C rats at 3, 6 and 9-mo, respectively (Heart: 54%, 50% and 57%; Gastrocnemius: 37%, 56% and 50%; Adipose tissue: 69%, 61% and 69%). CONCLUSIONS: MSG-treated SHR presented all metabolic syndrome characteristics, as well as reduced GLUT4 content, which must play a key role in the impaired glycemic homeostasis of the metabolic syndrome. BioMed Central 2012-08-16 /pmc/articles/PMC3439702/ /pubmed/22897936 http://dx.doi.org/10.1186/1475-2840-11-100 Text en Copyright ©2012 Leguisamo et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Investigation
Leguisamo, Natalia M
Lehnen, Alexandre M
Machado, Ubiratan F
Okamoto, Maristela M
Markoski, Melissa M
Pinto, Graziela H
Schaan, Beatriz D
GLUT4 content decreases along with insulin resistance and high levels of inflammatory markers in rats with metabolic syndrome
title GLUT4 content decreases along with insulin resistance and high levels of inflammatory markers in rats with metabolic syndrome
title_full GLUT4 content decreases along with insulin resistance and high levels of inflammatory markers in rats with metabolic syndrome
title_fullStr GLUT4 content decreases along with insulin resistance and high levels of inflammatory markers in rats with metabolic syndrome
title_full_unstemmed GLUT4 content decreases along with insulin resistance and high levels of inflammatory markers in rats with metabolic syndrome
title_short GLUT4 content decreases along with insulin resistance and high levels of inflammatory markers in rats with metabolic syndrome
title_sort glut4 content decreases along with insulin resistance and high levels of inflammatory markers in rats with metabolic syndrome
topic Original Investigation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3439702/
https://www.ncbi.nlm.nih.gov/pubmed/22897936
http://dx.doi.org/10.1186/1475-2840-11-100
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