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Combined effects of EFA deficiency and tumor necrosis factor‐α on circulating lipoproteins in rats
Author(s) -
Levy Emile,
Delvin Edgard,
Peretti Noel,
Bouchard Guylaine,
Seidman Ernest
Publication year - 2003
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/s11745-003-1103-z
Subject(s) - endocrinology , medicine , tumor necrosis factor alpha , lipoprotein lipase , lipid metabolism , clinical chemistry , very low density lipoprotein , adipose tissue , lipoprotein , lipidology , triglyceride , cholesterol , chemistry , biology
Both tumor necrosis factor‐α (TNF‐α) and EFA deficiency (EFAD) have been established as causes of marked perturbations in lipid and lipoprotein metabolism. Excessive levels of circulating TNF‐α 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‐α to EFAD rats. Lipoprotein lipase (LPL), the ratelimiting 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‐α, 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‐α treatment. In addition, TNF‐α modified lipoprotein‐lipid composition. VLDL and HDL 2 derived from EFAD rats were depleted in apolipoprotein (apo) E and apo A‐II, and enriched in apo A‐12 h after TNF‐α administration. Finally, TNF‐α decreased adipose tissue LPL activity in both control and EFAD animals. The TNF‐α‐induced inhibition was more marked in EFAD rats. The present results demonstrated that TNF‐α 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‐α on lipid metabolism.