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Is the Glucocorticoid-Induced Hypertriglyceridemia in Uremic Rats Caused by Decreased Tissue Lipoprotein Lipase Activity?

Mingpu Tan

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Abstract

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.

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What this paper is about

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.

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Available abstract

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 concepts: Internal medicine, Hypertriglyceridemia, Endocrinology, Lipoprotein lipase, Triglyceride, Triamcinolone acetonide, Adipose tissue, Adipose triglyceride lipase

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Is the Glucocorticoid-Induced Hypertriglyceridemia in Uremic Rats Caused by Decreased Tissue Lipoprotein Lipase Activity? — Research Paper | ScholarLens