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Islet‐activating protein discriminates the antilipolytic mechanism of insulin from that of other antilipolytic compounds
Author(s) -
Kather Horst,
Aktor Klaus,
Schulz Günter,
Jakobs Karl H.
Publication year - 1983
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(83)80749-2
Subject(s) - lipolysis , medicine , endocrinology , insulin , islet , cyclase , in vivo , adenylate kinase , nicotinic agonist , chemistry , prostaglandin e , prostaglandin e2 , adipose tissue , biology , stimulation , microbiology and biotechnology , receptor
In vivo administration of islet‐activating protein to rats resulted in an increase in fat cell lipolysis in vitro, which was associated with almost complete resistance of adipocytes towards the antilipolytic effects of N 6 ‐phenylisopropyladenosine, prostaglandin E 2 and nicotinic acid. Concomitantly, the inhibitory effects of these compounds on adenylate cyclase activity in membranes were impaired. In contrast, the antilipolytic action of insulin was not only preserved, but even augmented in cells from rats treated with islet‐activating protein. The data suggest that insulin exerts its antilipolytic effects via mechanisms which are different from those involved in the effects of prostaglandin E 2 , N 6 ‐phenylisopropyladenosine and nicotinic acid.