期刊
JOURNAL OF NUTRITIONAL SCIENCE AND VITAMINOLOGY
卷 60, 期 4, 页码 291-296出版社
CENTER ACADEMIC PUBL JAPAN
DOI: 10.3177/jnsv.60.291
关键词
equal; cAMP; protein kinase A signaling; enantioselectivity; pancreatic beta-cells
资金
- Japan Society for the Promotion of Science [23780141]
- Fuji Foundation for Protein Research
- Grants-in-Aid for Scientific Research [23780141] Funding Source: KAKEN
S-Equal is enantioselectively produced from the isoflavone daidzein by gut microflora and is absorbed by the body. An increase of pancreatic beta-cell death is directly associated with defects in insulin secretion and an increased risk of type 2 diabetes mellitus. In the present study, we demonstrate that only the S-enantiomer has suppressive effects against alloxan-induced oxidative stress in INS-1 pancreatic beta-cells. S-Equol reduced alloxan-induced cell death in a dose-dependent manner, whereas R-equol had no effects. In contrast, no significant differences were observed between the enantiomers in estrogenic activity. The cytoprotective effects of S-equol were stronger than those of its precursor daidzein and were blocked by the protein synthesis inhibitor cycloheximide. The cytoprotection was diminished when cells were incubated with a protein kinase A (PKA) inhibitor (H89), but not an estrogen receptor inhibitor. S-Equal increased intracellular cAMP levels in an enantioselective manner. S-Equol, but not R-equol, induced phosphorylation of cAMPresponse element-binding protein at Ser 133, and induced cAMP-response element-mediated transcription, both of which were diminished in the presence of H89. Taken together, these results show that S-equal enantioselectively increases the survival of INS-1 cells presumably through activating PICA signaling. Thus, S-equol might have applications as an anti-type 2 diabetic agent.
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