|Ronis, Martin -|
|Badeaux, Jamie -|
|Chen, Ying -|
Submitted to: Experimental Biology and Medicine
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 19, 2010
Publication Date: August 23, 2010
Citation: Ronis, M., Badeaux, J.V., Chen, Y., Badger, T.M. 2010. Rice Protein isolate improves lipid and glucose homeostasis in rats fed high fat/high cholesterol diets. Experimental Biology and Medicine. 235(9):1102-1113. Interpretive Summary: As the proportion of overweight children increases in the U.S., there is also increasing evidence of serious health effects secondary to obesity, known as “metabolic” syndrome, in children. This includes fatty liver disease, diabetes, and hypertension. Prevention or reversal of these diseases is a public health priority. Studies of Chinese and Japanese populations eating traditional diets demonstrate reduced risk of diabetes and heart disease compared to Westerners. Many studies have suggested this difference is due to soy protein consumption and the known effects of soy phytochemicals on fat and glucose metabolism and insulin sensitivity. However, there are many other diet differences between Asian and Western populations. One is the high consumption of rice products. The current study examines the health effects of rice protein isolate (RPI) (a rice product in widespread use in the food industry) on development of obesity and subsequent endocrine and metabolic disturbances after consumption of the high fat/high cholesterol “Western” diet. We demonstrated that feeding RPI to young rats increased breakdown of fatty acids and cholesterol in the liver. The fatty acid breakdown appeared to be triggered by some component of RPI being able to activate a liver transcription factor known as PPAR alpha, which regulates fat turnover. In longer term, studies in rats fed a “Western” style high fat/high cholesterol diet; fatty liver, increased serum cholesterol and development of insulin resistance were partly reversed by feeding RPI. These data are potentially important and suggest that substitution of plant proteins from rice and soy for animal proteins in children’s diet may prevent some of the health effects secondary to obesity.
Technical Abstract: Hundreds of phytochemicals are bound to rice protein isolate (RPI) and many are bioactive. To determine the metabolic effects of feeding RPI in early development, weanling rats were fed AIN-93G diets made with casein or RPI for 14 d. Reduced growth rate and adiposity prior to puberty in RPI-fed rats was associated with suppression of the growth hormone-insulin like growth factor 1 (GH-IGF1) axis. Peroxisome proliferator activated receptor (PPAR alpha) genes and proteins involved in fatty acid degradation were up-regulated by feeding RPI (P < 0.05), accompanied by increased promoter binding and nuclear expression of PPAR alpha and its heterodimerization partner RXR (P < 0.05). The effects on PPAR alpha signaling appeared to be direct and were reversed when RPI diets were switched to casein. Hepatic PPAR gamma signaling was up-regulated (P < 0.05) in RPI-fed rats, but this was less robust. RPI also increased expression of hepatic genes involved in cholesterol metabolism and transport. However RPI had no effect on binding of liver X-receptor (LXR)' to the cytochrome P450 (CYP) 7A1 promoter. In another experiment, male Sprague-Dawley rats were fed casein diets from post natal day 24 (PND24) to PND64 or were fed high fat “Western” diets containing 0.5% cholesterol and made with either casein or RPI. Increased liver triglyceride content, hypercholesterolemia and insulin resistance in the “Western” diet-fed rats were partially prevented by feeding RPI (P < 0.05). mRNA and protein expression of hepatic enzymes involved in fatty acid synthesis were suppressed by feeding “Western diets” containing RPI (P<0.05) despite a lack of effects on nuclear concentrations of sterol regulatory element binding protein (SREBP)-1c. These data suggest that attenuation of metabolic and endocrine effects observed in RPI-fed rats after consumption of “Western diets” was partly because of activation of PPARs.