|Linz, Amanda - ACNC|
|Xiao, Rijin - UAMS/ACNC|
|Parker, James - UAMS|
|Simpson, Pippa - UAMS|
|Badger, Thomas - UAMS/ACNC|
|Simmen, Frank - UAMS/ACNC|
Submitted to: Carcinogenesis
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 15, 2004
Publication Date: October 15, 2004
Citation: Linz, A.L., Xiao, R., Parker, J.G., Simpson, P.M., Badger, T.M., Simmen, F.A. 2004. Feeding of soy protein isolate to rats during pregnancy and lactation suppresses formatoin of aberrant crypt foci in their progeny's colons: interaction of diet with fetal alcohol exposure. Journal of Carcinogenesis. 3:14. Interpretive Summary: It is well unknown that many diseases that occur in adults were actually initiated very early in life. The ACNC has been studying some of these diseases and defining the relationship between early exposure to dietary factors, human development and prevention of diseases (both childhood and adult diseases). This study found that soy protein fed to the mom during pregnancy and lactation suppressed formation of certain types of colon cells that are precursors to colon cancer. Thus, this is an example of how very early dietary exposure to certain foods could help protect against colon cancer later in life. Future studies will expand these results and learn how this occurs.
Technical Abstract: Soy protein isolate (SPI) in the diet may inhibit colon tumorigenesis. We examined azoxymethane (AOM)-induced aberrant crypt foci (ACF) in male rats in relation to lifetime, pre-weaning, or post-weaning dietary exposure to SPI and within the context of fetal alcohol exposure. Pregnant Sprague-Dawley rats were fed AIN-93G diets containing casein (20%, the control diet) or SPI (20%) as the sole protein source starting on gestation day 4 (GD 4). Progeny were weaned on postnatal day (PND) 21 to the same diet as their dams and were fed this diet until termination of the experiment at PND 138. Rats received AOM on PND 89 and 96. Lifetime (GD 4 PND 138) feeding of SPI led to reduced frequency of ACF with 4 or more crypts in the distal colon. Progeny of dams fed SPI only during pregnancy and lactation or progeny fed SPI only after weaning exhibited similarly reduced frequency of large ACF in distal colon. The number of epithelial cells in the distal colon undergoing apoptosis was unaffected by diet. SPI reduced weight gain and adiposity, but these were not correlated with fewer numbers of large ACF. Lifetime SPI exposure inhibited development of large ACF in Sprague-Dawley rats whose dams were exposed to ethanol during pregnancy. In summary, feeding of SPI to rat dams during pregnancy and lactation led to suppression in numbers of large ACF in their progeny, implying a long-term or permanent change elicited by the maternal diet. Moreover, results support the use of ACF as an intermediate endpoint for elucidating effects of SPI and its biochemical constituents in colon cancer prevention in rat models.