title: Hypocholesterolemic effect of rice protein is due to regulating hepatic cholesterol metabolism in adult rats.
abstract: Aging is one of major risk factors for developing hypercholesterolemia. To elucidate the cholesterol-lowering mechanism exerted by rice protein (RP), the effects on hepatic cholesterol outputs and cholesterol metabolism related enzymes were investigated in adult rats, which were fed by casein (CAS) and RP without cholesterol in diets. After 2 weeks of feeding, the significant cholesterol-lowering effect was observed in adult rats fed by RP compared to CAS. The hepatic total- and VLDL-cholesterol secretions into circulation were significantly depressed in RP group, whereas biliary outputs of bile acids and cholesterol were effectively stimulated by RP-feeding, causing an increase in fecal sterol excretion compared to CAS. As a result, the apparent cholesterol absorption was significantly inhibited by RP. RP-feeding significantly increased the activity and gene expression of cholesterol 7α-hydroxylase, whereas acyl-CoA:cholesterol acyltransferase-2 activity and gene expression were significantly decreased by RP as compared with CAS. Neither activity nor gene expression of 3-hydroxy-3-methylglutaryl coenzyme A reductase of RP did differ from CAS in the liver. The present study demonstrates that rice protein can prevent hypercholesterolemia through modifying hepatic cholesterol metabolism under cholesterol-free dietary condition. The findings suggest that hypocholesterolemic action induced by rice protein is attributed in part to the inhibition of cholesterol absorption during the adult period.
authors.affiliation: Department of Food Science, School of Food Science and Engineering, Harbin Institute of Technology, 73 Huanghe Road, Harbin 150090, China. ly6617@hit.edu.cn
authors.forename: Lin
authors.initials: L
authors.lastname: Yang
authors.forename: Jia-Hou
authors.initials: JH
authors.lastname: Chen
authors.forename: Tong
authors.initials: T
authors.lastname: Xu
authors.forename: Ming-Hao
authors.initials: MH
authors.lastname: Nie
authors.forename: Hong-Kun
authors.initials: HK
authors.lastname: Yang
mesh_terms: D000375:Aging / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D000924:Anticholesteremic Agents / Q000737:chemistry / Q000494:pharmacology*; D002364:Caseins / Q000494:pharmacology; D015243:Cholesterol, VLDL / Q000378:metabolism*; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects / Q000502:physiology; D025782:Hydroxymethylglutaryl-CoA-Reductases, NADP-dependent / Q000096:biosynthesis; D008099:Liver / Q000378:metabolism*; D008297:Male; D012275:Oryza / Q000737:chemistry*; D014674:Plant Proteins, Dietary / Q000737:chemistry / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D002785:Sterol O-Acyltransferase / Q000096:biosynthesis; D000097587:Sterol O-Acyltransferase 2
chemical_list: D000924:Anticholesteremic Agents; D002364:Caseins; D015243:Cholesterol, VLDL; D025782:Hydroxymethylglutaryl-CoA-Reductases, NADP-dependent; D014674:Plant Proteins, Dietary; D002785:Sterol O-Acyltransferase; D000097587:Sterol O-Acyltransferase 2