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Thiamine reduced metabolic syndrome symptoms in rats via down-regulation of hepatic nuclear factor-kβ and induction activity of glyoxalase-I

OBJECTIVE(S): Metabolic syndrome (MS) is a cause of death worldwide. The hepatic nuclear factor- NF-kβ (NF-kβ) is the cardinal player of hepatic homeostasis, insulin sensitivity, and lipid metabolism. Thus, we investigated the effect of thiamine on hepatic gene expression of NF-kβ and its levels of...

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Autores principales: Mahdavifard, Sina, Dehghani, Razieh, Jeddi, Farhad, Najafzadeh, Nowruz
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Mashhad University of Medical Sciences 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8087849/
https://www.ncbi.nlm.nih.gov/pubmed/33995940
http://dx.doi.org/10.22038/ijbms.2021.53707.12086
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author Mahdavifard, Sina
Dehghani, Razieh
Jeddi, Farhad
Najafzadeh, Nowruz
author_facet Mahdavifard, Sina
Dehghani, Razieh
Jeddi, Farhad
Najafzadeh, Nowruz
author_sort Mahdavifard, Sina
collection PubMed
description OBJECTIVE(S): Metabolic syndrome (MS) is a cause of death worldwide. The hepatic nuclear factor- NF-kβ (NF-kβ) is the cardinal player of hepatic homeostasis, insulin sensitivity, and lipid metabolism. Thus, we investigated the effect of thiamine on hepatic gene expression of NF-kβ and its levels of activators in MS rats. MATERIALS AND METHODS: Male Wistar rats were randomly divided into 4 equal groups (ten rats in each group): normal, MS, and two alike groups under thiamine treatment. MS was induced in rats with a high sucrose solution (40 % in drinking water) for 4 months. Treated groups of rats received 0.18 % of thiamine daily in drinking water. Hematoxylin-Eosin stains were employed to determine the histopathological changes of the liver. Metabolic profile, glycation products, oxidative stress, inflammatory markers, the activity of glyoxalase-I, as well as NF-kβ hepatic expression of all rat groups, were determined. RESULTS: Acute hepatitis was not observed in the livers of the thiamine treated MS rats. Besides, the treatment showed an advantageous effect on glucose, lipid metabolism, and body weight via down-regulation of hepatic NF-kβ and induction of glyoxalase system activity. Furthermore, the treatment decreased diverse glycation, oxidative stress, and inflammatory markers (P>0.001). CONCLUSION: Thiamine decreased body weight and improved metabolism and activity of glyoxalase-I in MS rats with anti-glycation, antioxidant, and anti-inflammatory activities. Further, the treatment had a hepato-protective effect via reduction of NF-kβ signaling.
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spelling pubmed-80878492021-05-13 Thiamine reduced metabolic syndrome symptoms in rats via down-regulation of hepatic nuclear factor-kβ and induction activity of glyoxalase-I Mahdavifard, Sina Dehghani, Razieh Jeddi, Farhad Najafzadeh, Nowruz Iran J Basic Med Sci Original Article OBJECTIVE(S): Metabolic syndrome (MS) is a cause of death worldwide. The hepatic nuclear factor- NF-kβ (NF-kβ) is the cardinal player of hepatic homeostasis, insulin sensitivity, and lipid metabolism. Thus, we investigated the effect of thiamine on hepatic gene expression of NF-kβ and its levels of activators in MS rats. MATERIALS AND METHODS: Male Wistar rats were randomly divided into 4 equal groups (ten rats in each group): normal, MS, and two alike groups under thiamine treatment. MS was induced in rats with a high sucrose solution (40 % in drinking water) for 4 months. Treated groups of rats received 0.18 % of thiamine daily in drinking water. Hematoxylin-Eosin stains were employed to determine the histopathological changes of the liver. Metabolic profile, glycation products, oxidative stress, inflammatory markers, the activity of glyoxalase-I, as well as NF-kβ hepatic expression of all rat groups, were determined. RESULTS: Acute hepatitis was not observed in the livers of the thiamine treated MS rats. Besides, the treatment showed an advantageous effect on glucose, lipid metabolism, and body weight via down-regulation of hepatic NF-kβ and induction of glyoxalase system activity. Furthermore, the treatment decreased diverse glycation, oxidative stress, and inflammatory markers (P>0.001). CONCLUSION: Thiamine decreased body weight and improved metabolism and activity of glyoxalase-I in MS rats with anti-glycation, antioxidant, and anti-inflammatory activities. Further, the treatment had a hepato-protective effect via reduction of NF-kβ signaling. Mashhad University of Medical Sciences 2021-03 /pmc/articles/PMC8087849/ /pubmed/33995940 http://dx.doi.org/10.22038/ijbms.2021.53707.12086 Text en https://creativecommons.org/licenses/by/3.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/ (https://creativecommons.org/licenses/by/3.0/) ) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Mahdavifard, Sina
Dehghani, Razieh
Jeddi, Farhad
Najafzadeh, Nowruz
Thiamine reduced metabolic syndrome symptoms in rats via down-regulation of hepatic nuclear factor-kβ and induction activity of glyoxalase-I
title Thiamine reduced metabolic syndrome symptoms in rats via down-regulation of hepatic nuclear factor-kβ and induction activity of glyoxalase-I
title_full Thiamine reduced metabolic syndrome symptoms in rats via down-regulation of hepatic nuclear factor-kβ and induction activity of glyoxalase-I
title_fullStr Thiamine reduced metabolic syndrome symptoms in rats via down-regulation of hepatic nuclear factor-kβ and induction activity of glyoxalase-I
title_full_unstemmed Thiamine reduced metabolic syndrome symptoms in rats via down-regulation of hepatic nuclear factor-kβ and induction activity of glyoxalase-I
title_short Thiamine reduced metabolic syndrome symptoms in rats via down-regulation of hepatic nuclear factor-kβ and induction activity of glyoxalase-I
title_sort thiamine reduced metabolic syndrome symptoms in rats via down-regulation of hepatic nuclear factor-kβ and induction activity of glyoxalase-i
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8087849/
https://www.ncbi.nlm.nih.gov/pubmed/33995940
http://dx.doi.org/10.22038/ijbms.2021.53707.12086
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