Summary
The glucocorticoid-induced hypertriglyceridemia in uremic rats is partly due to defective
removal of triglyceride (Tg)-rich lipoproteins. To determine whether this was due
to decreased lipoprotein lipase (LPL), the key enzyme involved in the hydrolysis of
Tg-rich lipoproteins, the LPL activity in soleus, heart and adipose tissue and the
triglyceride secretion rates (TgSR) of uremic rats treated with Triamcinolone or placebo
were studied. Sprague-Dawley rats were made uremic by a 2-stage 5/6 nephrectomy and
studied three weeks later. During the 3rd week, one group was treated with a five
day course of Triamcinolone (0.5 mg/kg body weight i.m.) and the other given an equal
volume of saline. Triamcinolone aggravated the hypertriglyceridemia in uremic rats.
This was associated with an increase in soleus and heart LPL with no change in adipose
tissue LPL. The TgSR was also increased in the Triamcinolone-treated rats. These data
suggest that decreased LPL activity is not the cause of hypertriglyceridemia in these
rats.
Key-Words:
Uremic Hyperlipidemia
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Lipoprotein Lipase
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Glucocorticoid
