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ARS Home » Southeast Area » Little Rock, Arkansas » Microbiome and Metabolism Research Unit » Research » Publications at this Location » Publication #237258

Title: Soy protein isolate reduces hepatosteatosis in yellow Avy/a mice without altering coat color phenotype

Author
item BADGER, THOMAS - ACNC/UAMS
item RONIS, MARTIN - ACNC/UAMS
item WOLFF, GEORGE - ACNC/CONTRACT WORK
item STANLEY, STEVE - ACNC/UAMS
item FERGUSON, MATTHEW - ACNC
item SHANKAR, KARTIK - ACNC/UAMS
item SIMPSON, PIPPA - UAMS
item JO, CHAN - UAMS

Submitted to: Experimental Biology and Medicine
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/17/2008
Publication Date: 10/15/2008
Citation: Badger, T.M., Ronis, M.J., Wolff, G., Stanley, S., Ferguson, M., Shankar, K., Simpson, P.M., Jo, C.H. 2008. Soy protein isolate reduces hepatosteatosis in yellow Avy/a mice without altering coat color phenotype. Experimental Biology and Medicine. 233(10):1242-1254.

Interpretive Summary: The health effects of consuming soy foods has been called into question because of the potential actions of a class of soy compounds called isoflavones. One soy isoflavone is genistein, and it was shown that when fed to a genetically altered mouse (the Agouti mouse), genistein caused chances in gene expression and reduced obesity. This was said to be a condition that would also occur in infants who were fed soy infant formula. However, the effects of feeding purified genistein from the soy bean are not the same as feeding soy protein isolate, which is the protein in soy formula. Therefore, we conducted a study to determine if the same results could be observed in Agouti mice fed a diet that contained the same amount of genistein as the previous study, but with genistein supplied as part of the soy protein rather than being purified. The results showed very clearly that when genistein was fed at the same level, but as soy protein, there were no gene expression changes. Therefore, while the purified soy isolfavone genistein alters gene expression and reduced obesity in Agouti mice, this does not occur when genistein is supplied as part of the soy protein.

Technical Abstract: Agouti (Avy/a) mice fed an AIN-93G diet containing the soy isoflavone genistein (GEN) prior to and during pregnancy were reported to shift coat color and body composition phenotypes from obese-yellow towards lean pseudoagouti, suggesting epigenetic programming. Human consumption of purified GEN is rare, and soy protein is the primary source of GEN. Virgin a/a female and (Avy/a) male mice were fed AIN-93G diets made with casein (CAS) or SPI (the same approximate GEN levels as in the above mentioned study) for 2 wks prior to mating. (Avy/a) offspring were weaned to the same diets and studied at age 75 d. Coat color distribution did not differ among diets, but SPI-fed, obese (Avy/a) offspring had lower hepatosteatosis (P<0.05) and increased (P<0.05) expression of CYP4A, a PPAR-regulated gene, compared to CAS controls. Similarly, weanling male Sprague-Dawley (SD) rats fed SPI had elevated hepatic Acyl Co-A Oxidase (ACO) mRNA levels and increased in vitro binding of PPAR to the ACO gene response element. In another hepatosteatosis model, adult SD rats fed a high fat/cholesterol diet, SPI reduced (P<0.05) steatosis. Thus, 1) consumption of diets made with SPI partially protected against hepatosteatosis in yellow mice and in SD rats, and this may involve induction of PPAR-regulated genes; and 2) the lifetime (in utero, neonatal, and adult) exposure to dietary soy protein did not result in a shift in coat color phenotype of (Avy/a) mice. These findings, when compared with those of previously published studies of (Avy/a) mice, lead us to conclude that: 1) the effects of purified GEN differ from those of SPI when GEN equivalents are closely matched; 2) SPI does not epigenetically regulate the agouti locus to shift the coat color phenotype in the same fashion as GEN alone; and 3) SPI may be beneficial in management of non-alcoholic fatty liver disease.