ArticleLipids2003
Combined effects of EFA deficiency and tumor necrosis factor-alpha on circulating lipoproteins in rats.
Article in Lipids, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
0 citing papers in PubMed, 4 citations in OpenAlex.
No citing paper in PubMed yet.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both tumor necrosis factor-alpha (TNF-alpha) and EFA deficiency (EFAD) have been established as causes of marked perturbations in lipid and lipoprotein metabolism. Excessive levels of circulating TNF-alpha can coexist with EFAD in various clinical disorders such as cystic fibrosis and type I diabetes. The present study therefore aimed to investigate their combined effects on lipid profile and lipoprotein composition by administering TNF-alpha to EFAD rats. Lipoprotein lipase (LPL), the rate-limiting enzyme in TG catabolism, was also measured in epididymal adipose tissue. EFAD, after a 4-wk period, induced significant increases in plasma TG (80%, P < 0.001), total cholesterol (TC, 27%, P < 0.025), and HDL-cholesterol (HDL-C, 62%). Two hours after the administration of TNF-alpha, a further rise in TG (43%, P < 0.05) was noted in controls, but not EFAD animals. TC and HDL-C were unaffected by TNF-alpha treatment. In addition, TNF-alpha modified lipoprotein-lipid composition. VLDL and HDL2 derived from EFAD rats were depleted in apolipoprotein (apo) E and apo A-II, and enriched in apo A-I 2 h after TNF-alpha administration. Finally, TNF-alpha decreased adipose tissue LPL activity in both control and EFAD animals. The TNF-alpha-induced inhibition was more marked in EFAD rats. The present results demonstrated that TNF-alpha can amplify or antagonize the effects of EFAD on lipid profile, lipoprotein composition, and LPL activity. These data also suggest that the host's nutritional status is a determining factor for the modulating effect of TNF-alpha on lipid metabolism.
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