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Rapid downregulation of adipose tissue lipoprotein lipase activity on food deprivation: evidence that TNF- is involved

¹Department of Medical Biosciences, Physiological Chemistry, University of Umeå, SE-90187, Umeå, Sweden; and ²Department of Molecular Biomedical Research, VIB/Ghent University, B-9052 Ghent, Belgium

Submitted 10 June 2003 ; accepted in final form 12 December 2003

When food was removed from young rats in the early morning, adipose tissue tumor necrosis factor (TNF)- activity increased 50% and lipoprotein lipase (LPL) activity decreased 70% in 6 h. There was a strong negative correlation between the TNF- and LPL activities. Exogenous TNF- further decreased LPL activity. Pentoxifylline, known to decrease production of TNF-, had no effect on LPL activity in fed rats but almost abolished the rise of TNF- and the decrease of LPL activity in rats deprived of food. The specific activity of LPL decreased from 0.92 mU/ng in fed rats to 0.35 and 0.24 mU/ng in rats deprived of food given saline or TNF-, indicating a shift in the LPL molecules toward an inactive state. Lipopolysaccharide increased adipose tissue TNF- and decreased LPL activity. Both of these effects were strongly impeded by pretreatment of the rats with pentoxifylline, or dexamethasone. Pretreatment of the rats with actinomycin D virtually abolished the response of LPL activity to food deprivation or exogenous TNF-. We conclude that food deprivation, like lipopolysaccharide, signals via TNF- to a gene whose product causes a rapid shift of newly synthesized LPL molecules toward an inactive form and thereby shuts down extraction of lipoprotein triglycerides by the adipose tissue.

adipocytes; cytokines; endothelium; fasting; heparin; lipopolysaccharide; rat; secretion; tumor necrosis factor-

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