Alterations in thyroid status modulate apolipoprotein, hepatic triglyceride lipase, and low density lipoprotein receptor in rats.

The influence of altered thyroid state is investigated on plasma apolipoprotein-A-I (apo-A-I), apo-B, and apo-E levels and on apo-A-I, apo-A-II, apo-B, apo-E, hepatic triglyceride lipase (HTGL), and low density lipoprotein (LDL) receptor mRNA levels in rat liver and intestine. Plasma total cholesterol and triglycerides are unchanged in hyperthyroid rats. Liver apo-A-I mRNA levels increase 3-fold, whereas intestinal apo-A-I mRNA levels remain constant. Plasma apo-A-I levels almost double after L-T4. Liver apo-B and apo-E and intestinal apo-B mRNA levels are not influenced by L-T4, but plasma apo-B and apo-E decrease significantly. In the liver, apo-A-II mRNA levels decrease, whereas LDL receptor mRNA levels increase more than 50%. HTGL mRNA is not influenced by L-T4. N-Propyl-thiouracil-induced hypothyroidism does not influence plasma triglycerides, but plasma cholesterol levels nearly double. Liver and intestinal apo-A-I mRNA levels and plasma apo-A-I concentrations remain constant after propylthiouracil treatment. Accompanying the increase in plasma apo-B, liver and intestinal apo-B mRNA concentrations rise by approximately 100% and 40%, respectively. Plasma apo-E increases nearly 2-fold, but liver, apo-A-II mRNA rises, whereas HTGL and LDL receptor mRNA levels decrease 20% and nearly 50%, respectively. In conclusion, thyroid hormones regulate rat apo-A-I and apo-A-II gene expression in opposite directions. Furthermore, the LDL receptor is regulated at the mRNA level, whereas HTGL gene expression is relatively resistant to alterations in thyroid status.