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Am J Physiol Endocrinol Metab (December 23, 2003). doi:10.1152/ajpendo.00257.2003
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Submitted on June 10, 2003
Accepted on December 12, 2003

Rapid down-regulation of adipose tissue lipoprotein lipase activity on food deprivation. Evidence that TNF-{alpha} is involved

Gengshu Wu1, Peter Brouckaert2, and Thomas Olivecrona1*

1 Department of Medical Biosciences, Physiological Chemistry, University of Umea, Umea, Sweden
2 Department of Molecular Biomedical Research, VIB/Ghent University, Gent, Belgium

* To whom correspondence should be addressed. E-mail: Thomas.Olivecrona{at}medbio.umu.se.

When food was removed from young rats in the early morning, adipose tissue TNF-{alpha} activity increased 50 % and LPL activity decreased 70 % in six hours. There was a strong negative correlation between the TNF-{alpha} and LPL activities. Exogenous TNF-{alpha} further decreased LPL activity. Pentoxifylline, known to decrease production of TNF-{alpha}, had no effect on LPL activity in fed rats but almost abolished the rise of TNF-{alpha} 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-{alpha}, indicating a shift in the LPL molecules towards an inactive state. Lipopolysaccharide increased adipose tissue TNF-{alpha} and decreased LPL activity. Both of these effects were strongly impeded by pre-treatment of the rats with pentoxifylline, or dexamethasone. Pre-treatment of the rats with actinomycin D virtually abolished the response of LPL activity to food deprivation or exogenous TNF-{alpha}. We conclude that food deprivation, like lipopolysaccharide, signals via TNF-{alpha} to a gene whose product causes a rapid shift of newly-synthesized LPL molecules towards an inactive form and thereby shuts down extraction of lipoprotein triglycerides by the adipose tissue.




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