Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 2/6/2006
Publication Date: 3/27/2006
Citation: Ronis, M.J., Chen, Y., Badeaux, J., Badger, T.M. 2006. Feeding diets containing rice protein isolate (RPI) results in activation of hepatic PPAR and LXR-regulated genes in weanling rats [abstract]. The FASEB Journal. 20(4):A1015.
Interpretive Summary: Feeding rice protein isolate (RPI) has been reported to prevent the development of heart disease and to improve body composition by reducing % fat content in rats fed this protein source during development. The mechanisms remain unknown. In this study, we examined the effects of feeding RPI on genes involved in the breakdown of fatty acid (FA) and cholesterol, and on the movement of cholesterol into and out of cells on weanling rats. Rats fed high fat/high cholesterol diets and RPI had reduced liver fat accumulation; hepatic FA and cholesterol content (p < 0.05) relative to those fed casein. These data suggest that SPI increases hepatic FA and cholesterol breakdown and transport. In addition, we have determined that the mechanisms by which RPI works involved proteins (called transcription factors known as PPARs and LXR) important in regulation of genes that are essential for Cholesterol movement in and out of cells.
Technical Abstract: Feeding rice protein isolate (RPI) has been reported to prevent the development of atherosclerotic plaques in apoE knockout mice and to improve body composition indices in rats. The mechanisms remain unknown. The current study examined the effects of feeding (RPI) on expression of genes and transcription factors involved in fatty acid (FA) and cholesterol metabolism and transport. Sprague-Dawley rats were weaned onto AIN-93G diets containing RPI or casein (CAS) as the sole protein source from dams fed casein diets throughout gestation and lactation. At sacrifice on PND34, expression of PPAR'-regulated genes (acyl CoA oxidase (ACO), hydroxyacyl-Coenzyme A dehydrogenase, carnitine palmitoyltransferase); PPAR-regulated genes (glucokinase,, CD36) and LXR-regulated genes (CYP7A1, ABCA1, ABCG5, ABCG8) were induced (p < 0.05) by feeding RPI relative to expression in liver of those rats fed CAS as determined by real time RT-PCR. This was accompanied by increased binding of the PPAR''and PPAR' to their response elements on the ACO and glucokinase promoters as measured in EMSA and ChIP assays. Increased expression of PPAR mRNAs and apoprotein were also observed (p < 0.05). LXR binding to the CYP7A1 promoter was not significantly affected by feeding RPI. These data suggest that RPI increases hepatic FA and transport via induction of PPARs and increases cholesterol metabolism and transport more indirectly.