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J Biol Chem, Vol. 274, Issue 26, 18243-18251, June 25, 1999
From the The effects of acylation-stimulating protein
(ASP) and insulin on free fatty acid (FFA) release from isolated human
fat cells and the signal transduction pathways to induce these effects
were studied. ASP and insulin inhibited basal and
norepinephrine-induced FFA release by stimulating fractional FFA
re-esterification (both to the same extent) and by inhibiting FFA
produced during lipolysis (ASP to a lesser extent than insulin).
Protein kinase C inhibition influenced none of the effects of ASP or
insulin. Phosphatidylinositol 3-kinase inhibition counteracted the
effects of insulin but not of ASP. Phosphodiesterase 3 (PDE3) activity
was stimulated by ASP and insulin, whereas PDE4 activity was slightly
increased by ASP only. Selective PDE3 inhibition reversed the effects
of both ASP and insulin on fractional FFA re-esterification and
lipolysis. Selective PDE4 inhibition slightly counteracted the ASP but
not the effect of insulin on fractional FFA re-esterification and did
not prevent the action of ASP or insulin on lipolysis. Thus, ASP and
insulin play a major role in regulating FFA release from fat cells as
follows: insulin by stimulating fractional FFA re-esterification and
inhibiting lipolysis and ASP mainly by stimulating fractional FFA
re-esterification. For both ASP and insulin these effects on FFA
release are mediated by PDE3, and for ASP PDE4 might also be involved.
The signaling pathway preceding PDE is not known for ASP but involves
phosphatidylinositol 3-kinase for insulin.
Mechanisms Involved in the Regulation of Free Fatty Acid Release
from Isolated Human Fat Cells by Acylation-stimulating Protein and
Insulin
,,,
,
Department of Medicine and
Research Center, Huddinge University Hospital, Karolinska Institute,
S-141 86 Huddinge, Sweden, the § Mike Rosenbloom
Laboratory for Cardiovascular Research, Royal Victoria Hospital, McGill
University, Montreal, Quebec H3A 1A1, Canada, the ¶ Department
of Cell and Molecular Biology, Section for Molecular Signalling, Lund
University, S-221 00 Lund, Sweden, and the Department of
Surgery, Huddinge University Hospital, Karolinska Institute,
S-141 86 Stockholm, Sweden
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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