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J. Biol. Chem., Vol. 278, Issue 14, 11925-11930, April 4, 2003
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From the Department of Medical Biosciences, Physiological
Chemistry, Umeå University, SE-90185 Umeå, Sweden
Lipoprotein lipase (LPL) acts at the vascular
endothelium. Earlier studies have shown that down-regulation of adipose
tissue LPL during fasting is post-translational and involves a shift from active to inactive forms of the lipase. Studies in cell systems had indicated that during fasting LPL might be retained in the endoplasmic reticulum. We have now explored the relation between active/inactive and intra/extracellular forms of the lipase. Within adipocytes, neither LPL mass nor the distribution of LPL between active
and inactive forms changed on fasting. Extracellular LPL mass also did
not change significantly, but shifted from predominantly active to
predominantly inactive. To explore if changes in secretion were
compensated by changes in turnover, synthesis of new protein was
blocked by cycloheximide. The rates at which intra- and extracellular LPL mass and activity decreased did not change on fasting. To further
explore how LPL is distributed in the tissue, heparin (which detaches
the enzyme from the endothelial surface) was injected. Tissue LPL
activity decreased by about 10% in 2 min and by 50% in 1 h.
Heparin released mainly the active form of the lipase. There was no
change of LPL activity or mass within adipocytes. The fraction of
extracellular LPL that heparin released and the time course were the
same in fed and fasted rats, indicating that active, extracellular LPL
was distributed in a similar way in the two nutritional states. This
study suggests that the nutritional regulation of LPL in adipose tissue
determines the activity state of extracellular LPL.
The Distribution of Lipoprotein Lipase in Rat Adipose Tissue
CHANGES WITH NUTRITIONAL STATE ENGAGE THE EXTRACELLULAR
ENZYME*
*
This study was funded by the Swedish Medical Research
Council Grants 03X-00727 and 03X-12203.The costs of publication of this article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Fysiologisk Kemi,
Bldg. 6M, 3rd Floor, Umeå University, SE-90185 Umeå, Sweden. Tel.:
46-90-7854490; Fax: 46-90-7854496; Mobile: 46-70-2345839; E-mail:
Thomas.Olivecrona@medbio.umu.se.
Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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