EXOGENOUSLY HYPERCHOLESTEROLEMIC RATS, COMPARED WITH THEIR PROGENITORSPRAGUE-DAWLEY RATS, HAVE ALTERED MESSENGER-RNAS FOR CHOLESTEROL 7-ALPHA-HYDROXYLASE AND LOW-DENSITY-LIPOPROTEIN RECEPTOR AND ACTIVITIES OFCHOLESTEROL 7-ALPHA-HYDROXYLASE AND ACYL-COA - CHOLESTEROL ACYLTRANSFERASE IN THE LIVER IN RESPONSE TO DIETARY-CHOLESTEROL

Citation
K. Nagao et al., EXOGENOUSLY HYPERCHOLESTEROLEMIC RATS, COMPARED WITH THEIR PROGENITORSPRAGUE-DAWLEY RATS, HAVE ALTERED MESSENGER-RNAS FOR CHOLESTEROL 7-ALPHA-HYDROXYLASE AND LOW-DENSITY-LIPOPROTEIN RECEPTOR AND ACTIVITIES OFCHOLESTEROL 7-ALPHA-HYDROXYLASE AND ACYL-COA - CHOLESTEROL ACYLTRANSFERASE IN THE LIVER IN RESPONSE TO DIETARY-CHOLESTEROL, Comparative biochemistry and physiology. B. Comparative biochemistry, 118(4), 1997, pp. 949-955
Citations number
27
Categorie Soggetti
Biology,Zoology
ISSN journal
03050491
Volume
118
Issue
4
Year of publication
1997
Pages
949 - 955
Database
ISI
SICI code
0305-0491(1997)118:4<949:EHRCWT>2.0.ZU;2-T
Abstract
Exogenously hypercholesterolemic (ExHC) rats promptly increase serum c holesterol concentration in response to dietary cholesterol. To examin e underlying mechanism(s) for this susceptibility, responses of mRNAs for cholesterol metabolism-related proteins and their activities in th e liver to dietary cholesterol were compared between ExHC rats and the ir progenitor Sprague Dawley rats. ExHC rats slightly decreased the ab undance of low density lipoprotein (LDL) receptor mRNA in response to dietary cholesterol, although the amount of LDL receptor was not influ enced. The abundance of cholesterol 7 alpha-hydroxylase mRNA and the e nzyme activity in response to dietary cholesterol were greater in ExHC rats, but the fecal excretion of bile acid was comparable between the strain. Dietary cholesterol-dependent elevation of acyl-CoA:cholester ol acyltransferase activity was greater in ExHC rats. The concentratio n of liver triacylglycerols was markedly lower in ExHC rats. These res ults suggest that ExHC rats may increase serum cholesterol by increasi ng hepatic secretion of cholesteryl ester-rich particles. (C) 1997 Els evier Science Inc.