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This Article Full Text Full Text (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. J Search for Related Content PubMed PubMed Citation Articles by Singhal, R. Articles by Ronis, M. J

Rohit Singhal^1,, Kartik Shankar^1,3, Thomas M Badger^2,3

Departments of
¹ , Pharmacology and Toxicology
² Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, 72205 USA
³ Arkansas Children's Nutrition Center, 1120 Marshall Street, Little Rock, Arkansas 72202, USA

(Correspondence should be addressed to M J Ronis; Email: ronismartinj{at}uams.edu)

(R Singhal is now at Michigan State University, 222 Food Safety and Toxicology Building, East Lansing, Michigan 48824, USA)

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 17β-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 postnatal day (PND) 30. Rats were ovariectomized on PND 50 and infused with E₂ or vehicle in osmotic pumps for 14 d. 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, ±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 suggest that SPI is not estrogenic in these tissues.