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This Article Accepted manuscript (PDF) Supplementary data All Versions of this Article: JOE-09-0059v1 202/1/141    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Singhal, R. Articles by Ronis, M. Search for Related Content PubMed PubMed Citation Articles by Singhal, R. Articles by Ronis, M.

R Singhal, Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, 72202, United States
K Shankar, Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, United States
T Badger, Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, United States
M Ronis, Little Rock, United States

Correspondence: Rohit Singhal, Email: rohits149{at}gmail.com

Although soy foods have been recognized as an excellent source of protein, there have been recent concerns regarding potential adverse effects of isoflavone phytochemicals found in soy products, which are known to bind and activate estrogen receptors. Here we used global hepatic gene expression profiles in ovariectomized female Sprague-Dawley rats treated with 17beta-estradiol (E2) or fed with soy protein isolate (SPI) as a means of estimating potential estrogenicity of SPI. Female Sprague-Dawley rats were fed AIN-93G diets containing casein (CAS) or SPI starting at PND30. Rats were ovariectomized on PND50 and infused with E2 or vehicle in osmotic pumps for 14d. Microarray analysis was performed on liver using Affymetrix-GeneChip Rat 230 2.0. Serum E2 levels were within normal ranges for the rat and SPI feeding did not increase uterine wet weight in the absence or presence of E2. SPI feeding altered (P<0.05, more than 1.5 fold) the expression of 82 genes, while E2 treatment altered 892 genes. Moreover, only 4% of E2-affected genes were also modulated by SPI, including some whose expression was reversed by SPI feeding. The interaction between E2 and SPI uniquely modulated the expression profile of 225 genes including the reduction of those involved in fatty acid biosynthesis or glucocorticoid signaling and an induction of those involved in cholesterol metabolism. The different hepatic gene signatures produced by SPI-feeding compared with E2 and the lack of increase in uterine wet weight in rats fed with SPI suggests that SPI is not estrogenic in these tissues.