详细记录  
题名:Microbial phenolic metabolites improve glucose-stimulated insulin secretion and protect pancreatic beta cells against tert-butyl hydroperoxide-induced toxicity via ERKs and PKC pathways.
作者:FERNANDEZ-MILLAN E; RAMOS S; ALVAREZ C; BRAVO L; GOYA L; MARTIN MA;
来源:Food Chem Toxicol. 2014 Jan 31. pii: S0278-6915(14)00058-1. doi: [ IF= 0.00 ] ]
URL :10.1016/j.fct.2014.01.044
日期:20140217
摘要:Oxidative stress is accepted as one of the causes of beta cell failure in type 2
diabetes. Therefore, identification of natural antioxidant agents that preserve
beta cell mass and function is considered an interesting strategy to prevent or
treat diabetes. Recent evidences indicated that colonic metabolites derived from
flavonoids could possess beneficial effects on various tissues. The aim of this
work was to establish the potential anti-diabetic properties of the
microbial-derived flavonoid metabolites 3,4-dihydroxyphenylacetic acid (DHPAA),
2,3-dihydroxybenzoic acid (DHBA) and 3-hydroxyphenylpropionic acid (HPPA). To
this end, we tested their ability to influence beta cell function and to protect
against tert-butyl hydroperoxide-induced beta cell toxicity. DHPAA and HPPA were
able to potentiate glucose-stimulated insulin secretion (GSIS) in a beta cell
line INS-1E and in rat pancreatic islets. Moreover, pre-treatment of cells with
both compounds protected against beta cell dysfunction and death induced by the
pro-oxidant. Finally, experiments with pharmacological inhibitors indicate that
these effects were mediated by the activation of protein kinase C and the
extracellular regulated kinases pathways. Altogether, these findings strongly
suggest that the microbial-derived flavonoid metabolites DHPAA and HPPA may have
anti-diabetic potential by promoting survival and function of pancreatic beta
cells.

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