Protective effect of hydrogen sulfide on pancreatic beta-cells.
Nitric Oxide
; 46: 32-6, 2015 Apr 30.
Article
em En
| MEDLINE
| ID: mdl-25461273
ABSTRACT
Hydrogen sulfide (H2S) is recognized as a third gaseous signaling molecule behind nitric oxide (NO) and carbon monoxide (CO). In pancreatic beta-cells, H2S inhibits glucose-induced insulin release. There are multiple underlying mechanisms for this inhibitory process. Apart from these inhibitory effects, H2S also protects pancreatic islets from apoptotic cell death induced by high glucose. Moreover, expression of the H2S-producing enzyme, cystathionine γ-lyase (CSE), is induced by glucose stimulation. These observations suggest that H2S is produced in an inducible manner, as are the other two gaseous signaling molecules, NO and CO. We recently reported that a lack of CSE induces apoptotic beta-cell death and promotes the development of high-fat diet (HFD)-induced diabetes. These findings tempt us to suggest that H2S produced by CSE is part of a homeostatic mechanism used by pancreatic beta-cells to inhibit insulin release and reduce cellular stress evoked by glucose, possibly via the anti-oxidant properties of H2S.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Substâncias Protetoras
/
Células Secretoras de Insulina
/
Sulfeto de Hidrogênio
Limite:
Animals
/
Humans
Idioma:
En
Ano de publicação:
2015
Tipo de documento:
Article