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Proteolytic activity in the brain of alloxan diabetic rats: Presence of a proteolytic activator in the cerebral extract

BACKGROUND AND AIM: Diabetes mellitus is known to cause neurological disorders due to impaired glucose metabolism involving decreased utilization of glucose by the brain tissues. The mechanisms responsible for failure of glycemic regulation in type-2 diabetes leading to neurological impairment need...

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Detalles Bibliográficos
Autor principal: Nayeemunnisa
Formato: Texto
Lenguaje:English
Publicado: Medknow Publications 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2772018/
https://www.ncbi.nlm.nih.gov/pubmed/19902040
http://dx.doi.org/10.4103/0973-3930.44078
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author Nayeemunnisa,
author_facet Nayeemunnisa,
author_sort Nayeemunnisa,
collection PubMed
description BACKGROUND AND AIM: Diabetes mellitus is known to cause neurological disorders due to impaired glucose metabolism involving decreased utilization of glucose by the brain tissues. The mechanisms responsible for failure of glycemic regulation in type-2 diabetes leading to neurological impairment need to be thoroughly elucidated. MATERIALS AND METHODS: Type-2 diabetes was induced in albino rat models with alloxan monohydrate (40 mg/kg i.v.). Cerebral cortex and medulla oblongata were investigated 48 h after alloxan administration for the alterations in proteolytic activity. RESULTS: Diabetes caused an elevation (P < 0.001) of blood glucose and also proteolytic activity in the brain. CONCLUSION: Impaired glucose metabolism in the brain was the key factor which was responsible for the elevated (P < 0.001) proteolysis leading to brain dysfunction.
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spelling pubmed-27720182009-11-09 Proteolytic activity in the brain of alloxan diabetic rats: Presence of a proteolytic activator in the cerebral extract Nayeemunnisa, Int J Diabetes Dev Ctries Original Article BACKGROUND AND AIM: Diabetes mellitus is known to cause neurological disorders due to impaired glucose metabolism involving decreased utilization of glucose by the brain tissues. The mechanisms responsible for failure of glycemic regulation in type-2 diabetes leading to neurological impairment need to be thoroughly elucidated. MATERIALS AND METHODS: Type-2 diabetes was induced in albino rat models with alloxan monohydrate (40 mg/kg i.v.). Cerebral cortex and medulla oblongata were investigated 48 h after alloxan administration for the alterations in proteolytic activity. RESULTS: Diabetes caused an elevation (P < 0.001) of blood glucose and also proteolytic activity in the brain. CONCLUSION: Impaired glucose metabolism in the brain was the key factor which was responsible for the elevated (P < 0.001) proteolysis leading to brain dysfunction. Medknow Publications 2008 /pmc/articles/PMC2772018/ /pubmed/19902040 http://dx.doi.org/10.4103/0973-3930.44078 Text en © International Journal of Diabetes in Developing Countries http://creativecommons.org/licenses/by/2.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Nayeemunnisa,
Proteolytic activity in the brain of alloxan diabetic rats: Presence of a proteolytic activator in the cerebral extract
title Proteolytic activity in the brain of alloxan diabetic rats: Presence of a proteolytic activator in the cerebral extract
title_full Proteolytic activity in the brain of alloxan diabetic rats: Presence of a proteolytic activator in the cerebral extract
title_fullStr Proteolytic activity in the brain of alloxan diabetic rats: Presence of a proteolytic activator in the cerebral extract
title_full_unstemmed Proteolytic activity in the brain of alloxan diabetic rats: Presence of a proteolytic activator in the cerebral extract
title_short Proteolytic activity in the brain of alloxan diabetic rats: Presence of a proteolytic activator in the cerebral extract
title_sort proteolytic activity in the brain of alloxan diabetic rats: presence of a proteolytic activator in the cerebral extract
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2772018/
https://www.ncbi.nlm.nih.gov/pubmed/19902040
http://dx.doi.org/10.4103/0973-3930.44078
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