Islet-activating protein discriminates the antilipolytic mechanism of insulin from that of other antilipolytic compounds

FEBS Lett. 1983 Sep 5;161(1):149-52. doi: 10.1016/0014-5793(83)80749-2.


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 N6-phenylisopropyladenosine, prostaglandin E2 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 E2, N6-phenylisopropyladenosine and nicotinic acid.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Deaminase / metabolism
  • Adenylate Cyclase Toxin
  • Adenylyl Cyclases / metabolism
  • Adipose Tissue / drug effects
  • Adipose Tissue / metabolism*
  • Animals
  • Bacterial Proteins / pharmacology*
  • Dinoprostone
  • Glycerol / metabolism
  • Insulin / pharmacology*
  • Islets of Langerhans / drug effects*
  • Kinetics
  • Lipolysis / drug effects*
  • Male
  • Pertussis Toxin
  • Prostaglandins E / pharmacology
  • Rats
  • Theophylline / pharmacology
  • Virulence Factors, Bordetella


  • Adenylate Cyclase Toxin
  • Bacterial Proteins
  • Insulin
  • Prostaglandins E
  • Virulence Factors, Bordetella
  • Theophylline
  • Pertussis Toxin
  • Adenosine Deaminase
  • Adenylyl Cyclases
  • Dinoprostone
  • Glycerol