Amiodarone-induced hypercholesterolemia is associated with a decrease in liver LDL receptor mRNA

FEBS Lett. 1994 Mar 14;341(1):86-90. doi: 10.1016/0014-5793(94)80245-9.

Abstract

Amiodarone decreases plasma and tissue triiodothyronine (T3) 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 7 alpha-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 (approximately 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.

MeSH terms

  • Amiodarone / toxicity*
  • Animals
  • Cholesterol 7-alpha-Hydroxylase / biosynthesis
  • Cholesterol 7-alpha-Hydroxylase / metabolism
  • Hydroxymethylglutaryl CoA Reductases / genetics
  • Hydroxymethylglutaryl CoA Reductases / metabolism
  • Hypercholesterolemia / chemically induced*
  • Hypercholesterolemia / metabolism
  • Liver / drug effects*
  • Liver / metabolism
  • Male
  • Propylthiouracil / pharmacology
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Wistar
  • Receptors, LDL / genetics
  • Receptors, LDL / metabolism*
  • Time Factors

Substances

  • RNA, Messenger
  • Receptors, LDL
  • Propylthiouracil
  • Hydroxymethylglutaryl CoA Reductases
  • Cholesterol 7-alpha-Hydroxylase
  • Amiodarone