title: Rice protein isolate improves lipid and glucose homeostasis in rats fed high fat/high cholesterol diets.
abstract: In order to understand the molecular mechanisms underlying effects of feeding rice protein on lipid and glucose homeostasis, weanling rats were fed AIN-93G diets made with casein or rice protein isolate (RPI) for 14 d. Peroxisome proliferator-activated receptor (PPAR)alpha genes and proteins involved in fatty acid degradation were upregulated by feeding RPI (P < 0.05), accompanied by increased promoter binding and nuclear expression of PPARalpha and its heterodimerization partner retinoid X receptor (P < 0.05). Effects of RPI feeding on hepatic PPARgamma signaling were significant but less robust. Feeding RPI also increased hepatic genes involved in cholesterol metabolism and transport. However, feeding RPI had no effect on binding of liver X-receptor (LXR)alpha to the cytochrome P450 (CYP)7A1 promoter. The effect of RPI feeding on PPARalpha signaling appeared to be direct and was reversed when RPI diets were switched to casein. In another experiment, male Sprague-Dawley rats were fed casein diets from postnatal day (PND) 24 to PND64 or were fed high fat 'Western' diets containing 0.5% cholesterol 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-1c. These data suggest that attenuation of metabolic syndrome observed in RPI-fed rats after consumption of diets high in fat and cholesterol occur as a result of improved lipid and glucose homeostasis partly as a result of activation of PPARs.
authors.affiliation: Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, 15 Children's Way, Little Rock, AR 72202, USA. RonisMartinJ@uams.edu
authors.forename: Martin J
authors.initials: MJ
authors.lastname: Ronis
authors.forename: Jamie
authors.initials: J
authors.lastname: Badeaux
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
authors.forename: Thomas M
authors.initials: TM
authors.lastname: Badger
mesh_terms: D000818:Animals; D002784:Cholesterol / Q000032:analysis / Q000378:metabolism* / Q000494:pharmacology; D004032:Diet; D005223:Fats / Q000032:analysis / Q000378:metabolism / Q000494:pharmacology; D005947:Glucose / Q000032:analysis / Q000378:metabolism / Q000494:pharmacology; D006706:Homeostasis; D006937:Hypercholesterolemia / Q000378:metabolism; D007333:Insulin Resistance; D050356:Lipid Metabolism / Q000187:drug effects / Q000235:genetics; D008055:Lipids / Q000032:analysis / Q000494:pharmacology; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D000071518:Liver X Receptors; D008297:Male; D009765:Obesity / Q000378:metabolism; D057093:Orphan Nuclear Receptors / Q000378:metabolism; D012275:Oryza / Q000235:genetics / Q000378:metabolism; D047493:PPAR alpha / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D047495:PPAR gamma / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D011506:Proteins / Q000032:analysis / Q000378:metabolism / Q000494:pharmacology; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D047488:Retinoid X Receptors / Q000032:analysis / Q000378:metabolism / Q000494:pharmacology; D051780:Sterol Regulatory Element Binding Protein 1 / Q000235:genetics / Q000378:metabolism / Q000494:pharmacology
chemical_list: D005223:Fats; D008055:Lipids; D000071518:Liver X Receptors; C000605215:Nr1h3 protein, rat; D057093:Orphan Nuclear Receptors; D047493:PPAR alpha; D047495:PPAR gamma; D011506:Proteins; D012333:RNA, Messenger; D047488:Retinoid X Receptors; D051780:Sterol Regulatory Element Binding Protein 1; D002784:Cholesterol; D005947:Glucose