Linked Life Data

19100738

Source:http://linkedlifedata.com/resource/pubmed/id/19100738

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-1-22
pubmed:abstractText
We examined the expression of the major H(2)S-producing enzymes, cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE). CBS was ubiquitously distributed in the mouse pancreas, but CSE was found only in the exocrine. Freshly isolated islets expressed CBS, while CSE was faint. However, high glucose increased the CSE expression in the beta-cells. L-Cysteine or NaHS suppressed islet cell apoptosis with high glucose, and increased glutathione content in MIN6 beta-cells. Pretreatment with L-cysteine improved the secretory responsiveness following stimulation with glucose. The CSE inhibitor DL-propargylglycine antagonized these L-cysteine effects. We suggest H(2)S may function as an 'intrinsic brake' which protects beta-cells from glucotoxicity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1873-3468
pubmed:author
pubmed:issnType
Electronic
pubmed:day
22
pubmed:volume
583
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
377-82
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Glucose-induced production of hydrogen sulfide may protect the pancreatic beta-cells from apoptotic cell death by high glucose.
pubmed:affiliation
Department of Pharmacology, Oita University Faculty of Medicine, 1-1 Idaigaoka, Hasama, Oita 879-5593, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't