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Protective role of nano-selenium-enriched Bifidobacterium longum in delaying the onset of streptozotocin-induced diabetes

Bifidobacterium longum (B. longum) could accumulate Selenium (Se) and nano-Se in the form of Se-B. longum and Nano-Se-B. longum, respectively. In this study, the effect of Nano-Se-B. longum in diabetic mice was evaluated. Physiological and metabolic parameters such as blood glucose, body weight, ser...

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Autores principales: Lin, Yan, Ren, Yongzhe, Zhang, Yan, Zhou, Junjie, Zhou, Feng, Zhao, Quan, Xu, Genxing, Hua, Zichun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Royal Society 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6304152/
https://www.ncbi.nlm.nih.gov/pubmed/30662733
http://dx.doi.org/10.1098/rsos.181156
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author Lin, Yan
Ren, Yongzhe
Zhang, Yan
Zhou, Junjie
Zhou, Feng
Zhao, Quan
Xu, Genxing
Hua, Zichun
author_facet Lin, Yan
Ren, Yongzhe
Zhang, Yan
Zhou, Junjie
Zhou, Feng
Zhao, Quan
Xu, Genxing
Hua, Zichun
author_sort Lin, Yan
collection PubMed
description Bifidobacterium longum (B. longum) could accumulate Selenium (Se) and nano-Se in the form of Se-B. longum and Nano-Se-B. longum, respectively. In this study, the effect of Nano-Se-B. longum in diabetic mice was evaluated. Physiological and metabolic parameters such as blood glucose, body weight, serum insulin level, intraperitoneal glucose tolerance test (IPGTT), food intake, water consumption and urine output were evaluated. The expression of insulin signalling pathway-related proteins was evaluated by western blotting. Haematoxylin and eosin (H&E) was used for histological examination of the liver, pancreas and kidney sections. Creatinine levels in serum (SCr) and blood urea nitrogen (BUN) were measured. Nano-Se-B. longum was the best in terms of delaying the onset of diabetes. Nano-Se-B. longum decreased blood glucose and body weight compared with those noted for the model group. IPGTT, food intake, water consumption and urine output significantly increased and serum insulin levels significantly decreased in the model group compared with those in all the Nano-Se-B. longum-treated mice. Histological results showed that the Nano-Se-B. longum-treated mice were better than the model group mice in terms of pathological changes. The expression of insulin signalling pathway-related proteins was upregulated in the Nano-Se-B. longum-treated groups. A significant increase in SCr and BUN levels was noted in the model group. This study for the first time reported the dose-dependent preventive effect of Nano-Se-B. longum on the onset of diabetes and renal damage. The mechanism may be related to changes in insulin signalling.
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spelling pubmed-63041522019-01-18 Protective role of nano-selenium-enriched Bifidobacterium longum in delaying the onset of streptozotocin-induced diabetes Lin, Yan Ren, Yongzhe Zhang, Yan Zhou, Junjie Zhou, Feng Zhao, Quan Xu, Genxing Hua, Zichun R Soc Open Sci Biology (Whole Organism) Bifidobacterium longum (B. longum) could accumulate Selenium (Se) and nano-Se in the form of Se-B. longum and Nano-Se-B. longum, respectively. In this study, the effect of Nano-Se-B. longum in diabetic mice was evaluated. Physiological and metabolic parameters such as blood glucose, body weight, serum insulin level, intraperitoneal glucose tolerance test (IPGTT), food intake, water consumption and urine output were evaluated. The expression of insulin signalling pathway-related proteins was evaluated by western blotting. Haematoxylin and eosin (H&E) was used for histological examination of the liver, pancreas and kidney sections. Creatinine levels in serum (SCr) and blood urea nitrogen (BUN) were measured. Nano-Se-B. longum was the best in terms of delaying the onset of diabetes. Nano-Se-B. longum decreased blood glucose and body weight compared with those noted for the model group. IPGTT, food intake, water consumption and urine output significantly increased and serum insulin levels significantly decreased in the model group compared with those in all the Nano-Se-B. longum-treated mice. Histological results showed that the Nano-Se-B. longum-treated mice were better than the model group mice in terms of pathological changes. The expression of insulin signalling pathway-related proteins was upregulated in the Nano-Se-B. longum-treated groups. A significant increase in SCr and BUN levels was noted in the model group. This study for the first time reported the dose-dependent preventive effect of Nano-Se-B. longum on the onset of diabetes and renal damage. The mechanism may be related to changes in insulin signalling. The Royal Society 2018-12-12 /pmc/articles/PMC6304152/ /pubmed/30662733 http://dx.doi.org/10.1098/rsos.181156 Text en © 2018 The Authors. http://creativecommons.org/licenses/by/4.0/ Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, provided the original author and source are credited.
spellingShingle Biology (Whole Organism)
Lin, Yan
Ren, Yongzhe
Zhang, Yan
Zhou, Junjie
Zhou, Feng
Zhao, Quan
Xu, Genxing
Hua, Zichun
Protective role of nano-selenium-enriched Bifidobacterium longum in delaying the onset of streptozotocin-induced diabetes
title Protective role of nano-selenium-enriched Bifidobacterium longum in delaying the onset of streptozotocin-induced diabetes
title_full Protective role of nano-selenium-enriched Bifidobacterium longum in delaying the onset of streptozotocin-induced diabetes
title_fullStr Protective role of nano-selenium-enriched Bifidobacterium longum in delaying the onset of streptozotocin-induced diabetes
title_full_unstemmed Protective role of nano-selenium-enriched Bifidobacterium longum in delaying the onset of streptozotocin-induced diabetes
title_short Protective role of nano-selenium-enriched Bifidobacterium longum in delaying the onset of streptozotocin-induced diabetes
title_sort protective role of nano-selenium-enriched bifidobacterium longum in delaying the onset of streptozotocin-induced diabetes
topic Biology (Whole Organism)
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6304152/
https://www.ncbi.nlm.nih.gov/pubmed/30662733
http://dx.doi.org/10.1098/rsos.181156
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