详细记录  
题名:Endogenous hydrogen sulfide protects pancreatic beta-cells from a high-fat diet-induced glucotoxicity and prevents the development of type 2 diabetes.
作者:OKAMOTO M; YAMAOKA M; TAKEI M; ANDO T; TANIGUCHI S; ISHII I; TOHYA K; ISHIZAKI T; NIKI I; KIMURA T;
来源:Biochem Biophys Res Commun. 2013 Dec 13;442(3-4):227-33. doi: [ IF= 0.00 ] ]
URL :10.1016/j.bbrc.2013.11.023
日期:20140217
摘要:Chronic exposure to high glucose induces the expression of cystathionine
gamma-lyase (CSE), a hydrogen sulfide-producing enzyme, in pancreatic beta-cells,
thereby suppressing apoptosis. The aim of this study was to examine the effects
of hydrogen sulfide on the onset and development of type 2 diabetes. Middle-aged
(6-month-old) wild-type (WT) and CSE knockout (CSE-KO) mice were fed a high-fat
diet (HFD) for 8weeks. We determined the effects of CSE knockout on beta-cell
function and mass in islets from these mice. We also analyzed changes in gene
expression in the islets. After 8weeks of HFD, blood glucose levels were markedly
increased in middle-aged CSE-KO mice, insulin responses were significantly
reduced, and DNA fragmentation of the islet cells was increased. Moreover,
expression of thioredoxin binding protein-2 (TBP-2, also known as Txnip) was
increased. Administration of NaHS, a hydrogen sulfide donor, reduced TBP-2 gene
levels in isolated islets from CSE-KO mice. Gene levels were elevated when islets
were treated with the CSE inhibitor dl-propargylglycine (PPG). These results
provide evidence that CSE-produced hydrogen sulfide protects beta-cells from
glucotoxicity via regulation of TBP-2 expression levels and thus prevents the
onset/development of type 2 diabetes.

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