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Issue 2, 2013
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Anti-diabetic functions of soy isoflavone genistein: mechanisms underlying its effects on pancreatic β-cell function

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Abstract

Type 2 diabetes is a result of chronic insulin resistance and loss of functional pancreatic β-cell mass. Strategies to preserve β-cell mass and a greater understanding of the mechanisms underlying β-cell turnover are needed to prevent and treat this devastating disease. Genistein, a naturally occurring soy isoflavone, is reported to have numerous health benefits attributed to multiple biological functions. Over the past 10 years, numerous studies have demonstrated that genistein has anti-diabetic effects, in particular, direct effects on β-cell proliferation, glucose-stimulated insulin secretion and protection against apoptosis, independent of its functions as an estrogen receptor agonist, antioxidant, or tyrosine kinase inhibitor. Effects are structure-specific and not common to all flavonoids. While there are limited data on the effects of genistein consumption in humans with diabetes, there are a plethora of animal and cell-culture studies that demonstrate a direct effect of genistein on β-cells at physiologically relevant concentrations (<10 μM). The effects appear to involve cAMP/PKA signaling and there are some studies that suggest an effect on epigenetic regulation of gene expression. This review focuses on the anti-diabetic effects of genistein in both in vitro and in vivo models and potential mechanisms underlying its direct effects on β-cells.

Graphical abstract: Anti-diabetic functions of soy isoflavone genistein: mechanisms underlying its effects on pancreatic β-cell function

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Article information


Submitted
08 Aug 2012
Accepted
19 Oct 2012
First published
29 Oct 2012

Food Funct., 2013,4, 200-212
Article type
Review Article

Anti-diabetic functions of soy isoflavone genistein: mechanisms underlying its effects on pancreatic β-cell function

Elizabeth. R. Gilbert and D. Liu, Food Funct., 2013, 4, 200
DOI: 10.1039/C2FO30199G

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