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Two hypercholesterolemic mouse models, the apo-E–deficient mouse (Apoe −/− ) and the LDL receptor–deficient mouse (Ldlr −/− ), have been used extensively as animal models of atherogenesis. Total plasma cholesterol levels in chow-fedApoe −/− mice are much higher than inLdlr −/− mice. In a recent study, we managed to even-up the cholesterol levels inApoe −/− mice andLdlr −/− mice by making both models homozygous for theApob 100 (apo B-100–only) allele. On a chow diet, apo-E–deficient apo B-100–only mice (Apoe −/− Apob 100/100 ) and LDL receptor–deficient apo B-100–only mice (Ldlr −/− Apob 100/100 ) had similar total plasma cholesterol levels (≈300 mg/dL). The plasma ofLdlr −/− Apob 100/100 mice contained large numbers of small lipoproteins, whereas the plasma ofApoe −/− Apob 100/100 mice contained much lower levels of much larger lipoproteins. Interestingly, theLdlr −/− Apob 100/100 mice developed far more extensive atherosclerotic lesions than theApoe −/− Apob 100/100 mice. The finding of substantially more atherosclerosis inLdlr −/− Apob 100/100 mice than inApoe −/− Apob 100/100 mice, despite nearly identical cholesterol levels, suggests that large numbers of small apo B-100–containing lipoproteins are far more atherogenic than lower numbers of large apo B-100–containing lipoproteins.

Lipoprotein Size and Atherosclerosis Susceptibility in Apoe −/− and Ldlr −/− Mice

Lipoprotein Size and Atherosclerosis Susceptibility in Apoe ^−/− and Ldlr ^−/− Mice