IMR Press / FBE / Volume 3 / Issue 4 / DOI: 10.2741/E354

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Genistein stimulates the insulin-dependent signaling pathway
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1 Department of Health and Nutritional Science, Faculty of Human Health Science, Matsumoto University, 2095-1 Niimura, Matsumoto, Nagano 390-1295, Japan
2 Department of Bioscience and Biotechnology, Shinshu University, 8304 Minamiminowamura, Ina, Nagano 399-4598, Japan
3 Global COE Program, Nagoya University School of Medicine, Nagoya, Aichi 466-8550, Japan

*Author to whom correspondence should be addressed.


Front. Biosci. (Elite Ed) 2011, 3(4), 1534–1540;
Published: 1 June 2011

Small compounds that activate the insulin-dependent signaling pathway have potential therapeutic applications in controlling insulin-independent diabetes mellitus. In this study, we investigated whether soybean isoflavones could induce the expression of SHARP-2, a downstream component of insulin-dependent signaling pathway, associated with the regulation of blood glucose. One such compound called genistein, rapidly and temporarily induced SHARP-2 mRNA levels in a dose-dependent manner in rat H4IIE hepatoma cells. This induction process was rapidly stimulated by a protein kinase C (PKC) activator and blocked by a PKC inhibitor, suggesting that SHARP-2 may be induced via PKC activation. Upon Western blot analysis, genistein showed a stimulation of PKC phosphorylation. Therefore, we concluded that genistein might transcriptionally induce SHARP-2 through the activation of PKC in H4IIE cells. Our results suggest that genistein might be a useful dietary supplement to control insulin-independent diabetes mellitus by inducing the SHARP-2 expression via a bypass of the insulin-dependent signaling pathway.

Soybean Isoflavones
Signaling Pathway
Gene Expression
Classical Protein Kinase C
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