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Amiodarone‐induced hypercholesterolemia is associated with a decrease in liver LDL receptor mRNA
Author(s) -
Hudig F.,
Bakker O.,
Wiersinga W.M.
Publication year - 1994
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(94)80245-9
Subject(s) - endocrinology , medicine , propylthiouracil , amiodarone , triiodothyronine , ldl receptor , cholesterol , chemistry , messenger rna , receptor , reductase , thyroid , lipoprotein , enzyme , gene , biochemistry , atrial fibrillation
Amiodarone decreases plasma and tissue triiodothyronine (T 3 ) and increases plasma cholesterol levels resembling changes seen during hypothyroidism. To elucidate the mechanism of amiodarone‐induced hypercholesterolemia we investigated gene expression of three key proteins in cholesterol metabolism (cholesterol 7α‐hydroxylase, LDL receptor, HMG‐CoA reductase) in livers of rats. Animals were treated with amiodarone or propylthiouracil (to induce mild hypothyroidism). The LDL receptor mRNA was downregulated (≈50%) in both amiodarone‐treated and hypothyroid animals, while the other mRNA remained unchanged after 14‐day treatment. The results suggest that amiodarone‐induced hypercholesterolemia is associated with decreased LDL receptor mRNA levels.