Adrenergic blockade of hormone-induced lipolysis in isolated fat cells

Fain, J.N.

Annals of the New York Academy of Sciences 139(3): 879-890


ISSN/ISBN: 0077-8923
PMID: 4292399
DOI: 10.1111/j.1749-6632.1967.tb41257.x
Accession: 029916589

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The available evidence suggests that there are at least 3 different mechanisms for activation of lipolysis in fat cells: Catecholamines interact with a beta adrenergic receptor which results in a rapid activation of a triglyceride lipase. ACTH may act similarly but does not react with the same receptor site as catecholamines. The stimulation of lipolysis by growth hormone and glucocorticoid, on the other hand, occurs after a lag period of approxi-mately 1 to 2 hr. and appears to be mediated through a mechanism involving RNA and protein synthesis. Comparison of the effects of various drugs indicates that some drugs which have been described as adrenergic antagonists are actually nonspecific inhibitors of lipolysis. Insulin, nicotinic acid, and prostaglandin all inhibit basal lipolysis and the activation of lipolysis by all hormones tested. Alpha adrenergic blocking drugs, such as phenoxybenzamine, preferentially block the lipolytic action of growth hormone and glucocorticoids. An alpha blocking drug, such as phentolamine, will block the lipolytic action of epinephrine, but a beta blocking drug, such as propranolol, is about 300 times more potent as well as being a specific competitive antagonist of catecholamine-induced lipolysis with little effect on the lipolysis induced by other agents. The receptor for catecholamines in isolated fat cells should be classified as a beta adrenergic receptor on the basis of 1, the high potency and specificity of beta adrenergic blocking drugs as antagonists of catecholamine-induced lipolysis and 2, the order of potency of lipolytic effect of catecholamines, e.g. isoproterenol epinephrine and norepinephrine.