FAILURE OF THE NONSELECTIVE BETA-BLOCKER PROPRANOLOL TO AFFECT LIPOPROTEIN-LIPASE GENE-EXPRESSION IN THE RAT

Treatment with beta-blockers has been reported to be associated with t he development of hypertriglyceridemia. The etiology, even the existen ce, of this phenomenon is controversial. The purpose of our study was to examine whether the nonselective beta-blocker propranolol causes hy pertriglyceridemia in the rat and whether its action is mediated by th e modulation of lipoprotein lipase (LPL) messenger RNA (mRNA) accumula tion or activity. LPL activity was assayed in fresh tissue by incubati on with tritiated triglycerides. LPL mRNA was quantified in total RNA by slot-blot analysis using a mouse LPL complementary DNA probe. We ha ve conducted three series of experiments in unanaesthetized rats in or der to study the effects of different single doses of propranolol (1.5 to 6 mg i.p.) and different durations of treatment (15 min to 4 wk). We measured triglyceride and cholesterol levels in plasma as well as t he LPL activity and mRNA levels in the heart and adipose tissue before and after propranolol administration. In these experiments we did not find any significant decrease in either the activity or the amount of mRNA of lipoprotein lipase nor was there any change in plasma lipids following treatment. Our results lead us to the conclusion that the no nselective beta-blocker propranolol affects neither the activity nor t he mRNA level of LPL in the rat.