Insulin sensitizes β-agonist and forskolin-stimulated lipolysis to inhibition by 2′,5′-dideoxyadenosine

Yesim Gokmen-Polar, Elizabeth C. Coronel, Suleiman W. Bahouth, John N. Fain

Research output: Contribution to journalArticle

9 Scopus citations


In isolated rat adipocytes incubated in the absence of insulin, 2′,5′-dideoxyadenosine blocked the increase in total adenosine 3′,5′-cyclic monophosphate (cAMP) accumulation due to β1- or β3-catecholamine agonists and forskolin without affecting their stimulation of lipolysis. The inhibition of cAMP accumulation by 2′,5′-dideoxyadenosine was not reflected in the total cytosolic cAMP-dependent protein kinase A activity, suggesting that the inhibition of cAMP occurred in cellular compartments distinct from those involved in the regulation of bulk protein kinase A activity. However, there was a good correlation between effects of lipolytic agents on cytosolic protein kinase A activity in fat cell extracts and lipolysis. Furthermore, it was possible to see an inhibition of the increase due to β-agonists in cAMP accumulation, protein kinase A activity, and lipolysis by 2′,5′-dideoxyadenosine in the presence of insulin. These data suggest that the readily measurable accumulation of cAMP seen with catecholamines in the absence of insulin is in a compartment separate from that involved in protein kinase A activation.

Original languageEnglish (US)
Pages (from-to)C562-C569
JournalAmerican Journal of Physiology - Cell Physiology
Issue number2 39-2
StatePublished - Feb 1 1996
Externally publishedYes


  • Adenosine 3′,5′-cyclic monophosphate
  • Adipocytes
  • Catecholamines
  • Protein kinase A

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

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