Suppression of apolipoprotein AI gene expression in HepG2 cells by TNF α and IL-1β

Plasma inflammatory cytokines are elevated in obese subjects as well as in those with type 2 diabetes. This presumably results in systemic insulin resistance, characterized by a pro-atherogenic plasma lipid profile and reduced apolipoprotein AI (apoAI) protein levels. To determine how cytokine-media...

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Bibliographic Details
Published in:Biochimica et biophysica acta. General subjects 2003-10, Vol.1623 (2), p.120-128
Main Authors: Haas, Michael J, Horani, Mohammad, Mreyoud, Amjad, Plummer, Brian, Wong, Norman C.W, Mooradian, Arshag D
Format: Article
Language:English
Subjects:
Apolipoprotein AI
IL-1β
Insulin resistance
TNF α
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Summary:Plasma inflammatory cytokines are elevated in obese subjects as well as in those with type 2 diabetes. This presumably results in systemic insulin resistance, characterized by a pro-atherogenic plasma lipid profile and reduced apolipoprotein AI (apoAI) protein levels. To determine how cytokine-mediated insulin resistance suppresses apoAI gene expression, we investigated the effect of tumor necrosis factor α (TNF α) and interleukin-1β (IL-1β) on apoAI protein, mRNA, and transcriptional activity in the human hepatoma cell line HepG2. ApoAI secretion was suppressed in a dose-dependent manner in HepG2 cells treated with both cytokines. ApoAI protein levels were 2892±22.0, 2263±117, 2458±25.0, 3401±152, 2333±248, 1520±41.5 and 956.0±11.0 arbitrary units (AU) in cells treated with 0, 0.3, 1.0, 3.0, 10, 30, and 100 ng/ml TNF α, achieving statistical significance in the 30 and 100 ng/ml range ( P
ISSN:0304-4165
1872-8006
DOI:10.1016/j.bbagen.2003.08.004