Homozygous low-density lipoprotein receptor knock out mice (LDLR-/-) is a recognized model of atherosclerosis.28 Indeed, these mice develop spontaneous hyperc-holesterolemia with elevated levels of LDL and IDL and arteriosclerosis due to a genetic defect-deficiency of functional LDL receptors which is analogous to the genetic defects in humans with familial hypocholesterolemia.29,30 After 3 weeks of treatment and throughout the study that lasted for 16 weeks, LDLR-/- mice fed inulin (10% w/w of the high molecular weight HP product in diet) had a significantly lower concentration of plasma cholesterol (30%) but the same concentration of plasma TAGs compared to mice fed the standard diet.31 At the end of the protocol, the cholesterol content of VLDL, IDL, and LDL fractions of inulin-fed mice was lower (33, 40, 28%, respectively) than that of control mice. The concentration of cholesterol in HDL remained the same but the ratio HDL cholesterol over LDL cholesterol increased from 0.48 to 0.61 (1.280). Aortic arteriosclerosis expressed as the ratio intima/media tended to be lower (15%) in the inulin-fed than in the control mice but the difference was not statistically significant (p = 0.17).31
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