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Tri-iodothyronine prevents the amiodarone-induced decrease in the expression of the liver low-density lipoprotein
F Hudig1, O Bakker, W M Wiersinga
1Department of Endocrinology, University of Amsterdam, The Netherlands.
The Journal of Endocrinology
|March 1, 1997
Summary
Tri-iodothyronine (T3) administration prevents amiodarone-induced increases in plasma cholesterol by restoring liver low-density lipoprotein (LDL) receptors. This suggests amiodarone
Area of Science:
- Pharmacology
- Endocrinology
- Molecular Biology
Background:
- Amiodarone, an antiarrhythmic drug, increases plasma cholesterol by reducing liver low-density lipoprotein (LDL) receptors.
- This effect is similar to hypothyroidism, suggesting amiodarone may induce a local hypothyroid-like state.
Purpose of the Study:
- To investigate if exogenous tri-iodothyronine (T3) can counteract amiodarone's effects on LDL cholesterol.
- To explore the role of T3 in amiodarone's impact on LDL receptor expression.
Main Methods:
- Rats were treated with amiodarone, amiodarone plus varying doses of T3, or T3 alone.
- Plasma LDL cholesterol, liver LDL receptor mRNA, and protein levels were measured.
- Liver T3 content was also assessed.
Main Results:
- Amiodarone significantly increased plasma LDL cholesterol and decreased liver LDL receptors and mRNA.
- T3 administration dose-dependently reversed these amiodarone-induced changes.
- T3 alone decreased plasma LDL cholesterol and increased LDL receptor mRNA expression.
Conclusions:
- Exogenous T3 effectively prevents amiodarone's adverse effects on LDL cholesterol and liver LDL receptor expression.
- The findings indicate that amiodarone's inhibition of LDL receptor gene expression is mediated by T3-dependent pathways.
- This research highlights a potential therapeutic strategy involving T3 to manage amiodarone-induced hypercholesterolemia.