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We have previously observed that cholesterol-fed dogs with plasma cholesterol levels of 350 to 750 mg/dl failed to develop atherosclerosis (hyporesponders), whereas cholesterol-fed dogs with cholesterol levels greater than 750 mg/dl developed markedly accelerated atherosclerosis (hyperresponders). Two striking features of the hypercholesterolemia of the hyperresponders were the occurrence of cholesteryl ester-rich, β-mlgrating very low density llpoproteins (β-VLDL) In the d < 1.006 fraction and a decrease in plasma concentration of typical high density llpoproteins (HDL). Cholesterol-induced β-VLDL have been shown to cause massive accumulations of cholesteryl esters in mouse peritoneal macrophages in vitro, and HDL have been shown to remove cholesterol from these cells. In the present study, the mouse peritoneal macrophage system was used to explore the effects of high levels of cholesterol-Induced d < 1.006 llpoproteins and low levels of HDL In mediating cholesteryl ester synthesis and accumulation In these cells. It was found that the d < 1.006 lipoproteins from both the atherosclerotic hyperresponders and the nonatherosclerotlc hyporesponders stimulated cholesteryl [
Arteriosclerosis – Wolters Kluwer Health
Published: Mar 1, 1982
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