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Possible Role of Hydrogen Sulfide in Insulin Secretion and in Development of Insulin Resistance

H(2)S has been proposed as physiological important molecule. It is considered as first endogenous gaseous K(+) channel opener. K(+) ATP channel activity is mainly responsible for insulin secretion. K(+)ATP channel opening of β cells leads to inhibition of insulin secretion and channels closing leads...

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Detalles Bibliográficos
Autores principales: Patel, MA, Shah, GB
Formato: Texto
Lenguaje:English
Publicado: Medknow Publications 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3021689/
https://www.ncbi.nlm.nih.gov/pubmed/21264117
http://dx.doi.org/10.4103/0975-1483.63156
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author Patel, MA
Shah, GB
author_facet Patel, MA
Shah, GB
author_sort Patel, MA
collection PubMed
description H(2)S has been proposed as physiological important molecule. It is considered as first endogenous gaseous K(+) channel opener. K(+) ATP channel activity is mainly responsible for insulin secretion. K(+)ATP channel opening of β cells leads to inhibition of insulin secretion and channels closing leads to secretion. H2S is the gaseous K(+) ATP channel opener but it does not have channel specificity. So, H(2)S may have some effect on insulin secretion. H(2)S is high in Zuker diabetic fatty rats. That means H(2)S is high in insulin resistance condition. We tried to find out the role of H(2)S in insulin secretion and in development of insulin resistance. From the result of our study, H(2)S have K(+) ATP channel opening activity on β cells. H(2)S does not have any role in the development of insulin resistance. Decrease in insulin level in Zuker diabetic rat and streptozotocin-induced diabetic rat is due to high H(2)S level.
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spelling pubmed-30216892011-01-24 Possible Role of Hydrogen Sulfide in Insulin Secretion and in Development of Insulin Resistance Patel, MA Shah, GB J Young Pharm Pharmacology H(2)S has been proposed as physiological important molecule. It is considered as first endogenous gaseous K(+) channel opener. K(+) ATP channel activity is mainly responsible for insulin secretion. K(+)ATP channel opening of β cells leads to inhibition of insulin secretion and channels closing leads to secretion. H2S is the gaseous K(+) ATP channel opener but it does not have channel specificity. So, H(2)S may have some effect on insulin secretion. H(2)S is high in Zuker diabetic fatty rats. That means H(2)S is high in insulin resistance condition. We tried to find out the role of H(2)S in insulin secretion and in development of insulin resistance. From the result of our study, H(2)S have K(+) ATP channel opening activity on β cells. H(2)S does not have any role in the development of insulin resistance. Decrease in insulin level in Zuker diabetic rat and streptozotocin-induced diabetic rat is due to high H(2)S level. Medknow Publications 2010 /pmc/articles/PMC3021689/ /pubmed/21264117 http://dx.doi.org/10.4103/0975-1483.63156 Text en © Journal of Young Pharmacists 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 Pharmacology
Patel, MA
Shah, GB
Possible Role of Hydrogen Sulfide in Insulin Secretion and in Development of Insulin Resistance
title Possible Role of Hydrogen Sulfide in Insulin Secretion and in Development of Insulin Resistance
title_full Possible Role of Hydrogen Sulfide in Insulin Secretion and in Development of Insulin Resistance
title_fullStr Possible Role of Hydrogen Sulfide in Insulin Secretion and in Development of Insulin Resistance
title_full_unstemmed Possible Role of Hydrogen Sulfide in Insulin Secretion and in Development of Insulin Resistance
title_short Possible Role of Hydrogen Sulfide in Insulin Secretion and in Development of Insulin Resistance
title_sort possible role of hydrogen sulfide in insulin secretion and in development of insulin resistance
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3021689/
https://www.ncbi.nlm.nih.gov/pubmed/21264117
http://dx.doi.org/10.4103/0975-1483.63156
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