|Singhal, Rohit -|
|Shankar, Kartik -|
|Badger, Thomas -|
|Ronis, Martin -|
Submitted to: Journal of Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: April 15, 2009
Publication Date: June 15, 2009
Citation: Singhal, R., Shankar, K., Badger, T.M., Ronis, M.J. 2009. Hepatic gene expression following consumption of soy protein isolate in female sprague-dawley rats differs from that produced by 17beta-estradiol treatment. Journal of Endocrinology. 202(1):141-152. Interpretive Summary: The major issues raised by some scientists concerning the health effects of soy foods relates to the actions of isoflavones. Some say that isoflavones act as estrogens and therefore soy consumption presents a danger to children and women. In this study we addressed the effects of soy protein isolate (SPI, the protein used in soy infant formula) and compared them to the effects of estradiol (the major estrogen circulating in women). Estrogens act primarily through regulating gene expression (turning on or off genes), so we studied genes that were affected by estradiol or SPI. We found that SPI does not act as an estrogen, but rather has a specific gene expression profile and this profile is uniquely different from that of estradiol. Therefore, soy foods are not likely to have estrogenic effects.
Technical Abstract: 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 the 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.