Hypertriglyceridemia and Lipoprotein Lipase Activity in Experimental Uremia

Kraemer, Fredric B.; Chen, Yii‐Der I.; Reaven, Gerald M.

doi:10.1159/000182490

Cited by 10 publications

(6 citation statements)

References 6 publications

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“…The results of the present study in chronically uremic rats confirm the well-known disturbed metabolism of TG-rich particles, decreased LPL activity of epididymal fat tissue, and increased concentrations of serum total Choi and choline-PLas previously reported [13,14,18,19]. In this experimental model of uremia thyroid dysfunc tion is reflected by a decrease in serum total T4 concentra tion associated with a normal serum total T, level, sim ilarly to the results obtained by Lim et al [1] in rats 5 weeks after initiating chronic renal failure.…”

Section: Discussionsupporting

confidence: 92%

Chronic Triiodothyronine Supplementation Does Not Improve the Lipoprotein Disorders of Mildly Uremic Rats

Lacour

Roullet²,

Ricordel

et al. 1987

Nephron

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The present study was performed to appreciate the potential role that thyroid deficiency could play in the energy homeostasis and lipid metabolism of experimental chronic renal failure. For this purpose, 12 uremic rats that were supplemented with T₃ (0.4 μg/100 g body weight/day) during 5 weeks by means of osmotically driven minipumps were compared to 12 unsupplemented uremic rats and 12 control rats. The chronic supplementation of uremic rats with T₃ induced no significant change in body weight gain or in the serum concentration of insulin, glucose, glycerol, nonesterified fatty acids, total triglycerides (TG), total cholesterol, and total choline phospholipids. Similarly, the metabolism of TG-rich lipoproteins was not affected by the supplementation with T₃ in these uremic rats as appreciated by TG production or TG degradation (adipose tissue lipoprotein lipase activity). T₃ administration induced a significant decrease in serum β-hydroxybutyrate concentration and an increase in serum lactate concentration. Furthermore, heparin-releasable hepatic TG lipase activity as expressed per total liver mass was decreased in uremic rats treated with T₃. The latter changes were observed in the absence of modifications of serum glucose or TG concentration. We conclude from these observations that rats with a moderate degree of chronic uremia do not seem to have a cellular thyroid deficiency sufficient to disturb their energy or lipid metabolism.

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Section: Discussionsupporting

confidence: 92%

Chronic Triiodothyronine Supplementation Does Not Improve the Lipoprotein Disorders of Mildly Uremic Rats

Lacour

Roullet²,

Ricordel

et al. 1987

Nephron

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“…Decreased LPL activity can cause elevation of these Tg-rich lipoproteins (Havel 1965). Decreased heparin-releasable adipose tissue LPL activity has been reported in the uremic rat but there was no correlation between this LPL activity and the plasma Tg (Kraemer et al 1982). Our data corroborate those of others (Bagdade, Yee, Wilson and Shafrir 1978) in showing the adipose tissue LPL to be unaffected by uremia.…”

Section: Discussionsupporting

confidence: 89%

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

Ming¹

1985

Horm Metab Res

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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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“…i protein lipase (Kraemer et al, 1982) and hepatic triglyceride lipase (Mordasini et al, 1977) (Anderson & Norbeck, 1981) and even with the reduced dosage employed in this study drug levels far in excess of this recommended level were attained.…”

Section: Significant Elevations In Serum Creatininementioning

confidence: 61%

The short term effects of bezafibrate on the hypertriglyceridaemia of moderate to severe uraemia.

Ar¹,

Baker²,

Walls³

1984

Brit J Clinical Pharma

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Hypertriglyceridaemia, an atherogenic risk factor, is a well recognised complication of uraemia, and is present in the earliest stages of the disease. Bezafibrate is an effective hypolipidaemic agent, and its effect in moderate to severe uraemia is documented in this study. Significant reductions in serum triglyceride and cholesterol have been achieved after 1 month's therapy with a reduced dosage of bezafibrate. A reduction in the hyperinsulinaemia was also seen, but no change in the fractional removal rate of injected lipid emulsion (K2) was observed. An accelerated decline in some patients' renal function was observed, which was partially reversed on cessation of treatment. Reversible elevations in the serum creatinine phosphokinase were also seen, but no patient exhibited the myositis‐like syndrome associated with clofibrate.

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Hypertriglyceridemia and Lipoprotein Lipase Activity in Experimental Uremia

Cited by 10 publications

References 6 publications

Chronic Triiodothyronine Supplementation Does Not Improve the Lipoprotein Disorders of Mildly Uremic Rats

Chronic Triiodothyronine Supplementation Does Not Improve the Lipoprotein Disorders of Mildly Uremic Rats

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

The short term effects of bezafibrate on the hypertriglyceridaemia of moderate to severe uraemia.

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