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Journal of Lipid Research, Vol 34, 923-931, Copyright © 1993 by Lipid Research, Inc.
S Dueland, J Drisko, L Graf, D Machleder, AJ Lusis and RA Davis
Compared to BALB/c mice, inbred C57BL/6 mice are more susceptible to
developing fatty streak atherosclerotic lesions when fed a cholesterol-
rich diet containing taurocholate. We examined the metabolic basis for the
taurocholate requirement. In contrast to widely accepted assumptions,
taurocholate did not increase cholesterol absorption in either strain of
mouse. However, in susceptible C57BL/6 mice, taurocholate was required to
increase plasma concentrations of apoB. In both strains, the
cholesterol-rich diet increased both the activity and mRNA for 7
alpha-hydroxylase, a compensatory response to maintain cholesterol
homeostasis. In both strains, adding taurocholate to the diet suppressed
both the activity and mRNA for 7 alpha-hydroxylase, thus blocking this
important compensatory response. The cholesterol- rich diet (without
taurocholate) significantly increased hepatic cholesterol content in both
strains of mice, but repressed low density lipoprotein (LDL) receptor mRNA
only in BALB/c mice (not in C57BL/6 mice). However, adding taurocholate to
the cholesterol-rich diet did decrease LDL receptor mRNA in C57BL/6 mice.
In C57BL/6, but not in BALB/c mice, there was a linear parallel
relationship between 7 alpha- hydroxylase mRNA and LDL receptor mRNA. These
data show the existence of strain-specific differences in the effects of
dietary cholesterol and taurocholate on 7 alpha-hydroxylase and LDL
receptor expression. The combined data suggest that genetic factors
determine how the expression of hepatic LDL receptors responds to dietary
cholesterol and taurocholate.
ARTICLES
Effect of dietary cholesterol and taurocholate on cholesterol 7 alpha- hydroxylase and hepatic LDL receptors in inbred mice
Atherosclerosis Research Center, University of Colorado Health Sciences Center, Denver 80262.
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