Lipolysis by human adipose tissue: the role of cyclic 3',5'-adenosine monophosphate and adrenergic receptor sites.

Abstract

Abstract The basal lipolytic activity of isolated human adipose tissue cells was greatly stimulated by dibutyryl cyclic adenosine monophosphate (DAMP) or theophylline. Insulin reduced but did not abolish the enhanced lipolysis due to DAMP and theophylline. Epinephrine, a mixed adrenergic receptor site agonist, and isoproterenol, a beta site agonist, were incubated with human cells and rat cells, alone and in combination with an alpha site blocker, phentolamine, and a beta site blocking agent, propranolol. Neither phentolamine alone nor propranolol alone influenced lipolysis by either human or rat cells. With human cells, epinephrine plus phentolamine further increased the lipolytic response prompted by epinephrine alone, while epinephrine plus propranolol caused depression of lipolysis below the basal level. With rat cells, phentolamine had no effect on epinephrine-stimulated lipolysis and propranolol abolished it. With both human and rat cells, isoproterenol, on an equimolar basis, was more potent than epinephrine; lipolysis stimulated by isoproterenol was unaffected by phentolamine and was abolished by propranolol. These results are interpreted to indicate that both alpha and beta sites are present in human adipose tissue and act in a divergent manner in mediating the effects of epinephrine, while only beta sites could be demonstrated in rat cells. With human cells, lipolysis stimulated by thyroid-stimulating hormone (TSH) and a related human pituitary fraction (DEAE II) was not influenced by either propranolol or phentolamine but was decreased when alpha sites were stimulated with epinephrine plus propranolol.