TY - JOUR
T1 - Defective Lipoprotein Receptors and Atherosclerosis
T2 - Lessons from an Animal Counterpart of Familial Hypercholesterolemia
AU - Goldstein, J. L.
AU - Kita, T.
AU - Brown, M. S.
PY - 1983/8/4
Y1 - 1983/8/4
N2 - In 1913, Anitschkow fed cholesterol to rabbits, and thereby demonstrated that a high blood level of cholesterol can produce atherosclerosis in animals just as it can in human beings — with one fundamental difference. Human hypercholesterolemia is caused by genetic or acquired abnormalities in the synthesis or degradation of plasma lipoproteins that shuttle endogenous cholesterol between body tissues; dietary cholesterol is only an indirect aggravating factor. In laboratory animals hypercholesterolemia is produced exogenously when the normal mechanisms of lipoprotein clearance are overwhelmed by large amounts of dietary cholesterol. Since dietary and endogenous cholesterol are transported by different plasma lipoproteins, the.
AB - In 1913, Anitschkow fed cholesterol to rabbits, and thereby demonstrated that a high blood level of cholesterol can produce atherosclerosis in animals just as it can in human beings — with one fundamental difference. Human hypercholesterolemia is caused by genetic or acquired abnormalities in the synthesis or degradation of plasma lipoproteins that shuttle endogenous cholesterol between body tissues; dietary cholesterol is only an indirect aggravating factor. In laboratory animals hypercholesterolemia is produced exogenously when the normal mechanisms of lipoprotein clearance are overwhelmed by large amounts of dietary cholesterol. Since dietary and endogenous cholesterol are transported by different plasma lipoproteins, the.
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U2 - 10.1056/NEJM198308043090507
DO - 10.1056/NEJM198308043090507
M3 - Review article
C2 - 6306464
AN - SCOPUS:0020967144
SN - 0028-4793
VL - 309
SP - 288
EP - 296
JO - New England Journal of Medicine
JF - New England Journal of Medicine
IS - 5
ER -