title: Inhibition of fatty acid synthesis by stimulation of alpha- and beta-adrenergic receptors in human mononuclear leukocytes.
abstract: Selective alpha- and beta-adrenergic agonists and antagonists were used to determine the action of catecholamines on fatty acid biosynthesis in freshly isolated human mononuclear leukocytes. Incubation of cells for 22 h in a lipid-free medium resulted in a 4-fold increase in the incorporation of [14C]acetate into fatty acids. Addition of (-)-epinephrine in increasing concentrations to the incubation medium inhibited the rate of fatty acid synthesis by 42% at a concentration of 0.1 M. Similar effects were observed using (-)-norepinephrine and the beta-agonist isoproterenol. The catecholamine action was diminished by the unselective beta-blocker propranolol and mimicked by dibutyryl cyclic AMP. Since human mononuclear leukocytes possess beta 2-, but not beta 1-adrenoceptors (Brodde, Engel and Hoyer 1981), catecholamines may act via beta-adrenergic receptors of the beta 2-subtype. In addition, it appears that stimulation of alpha-adrenergic receptors inhibits fatty acid synthesis, too. In the presence of a beta-blockade by 1 microM propranolol, the alpha 2-agonist alpha-methylnorepinephrine, but not the alpha 1-agonist phenylephrine inhibited fatty acid synthesis rate. Accordingly, the epinephrine effect was attenuated by the alpha 2-antagonist yohimbine, but not by the alpha 1-antagonist prazosin. The results provide evidence that catecholamines may inhibit the synthesis rate of fatty acids by stimulation of both, beta 2- and alpha 2-adrenergic receptors.
authors.affiliation: Klinik II and Poliklinik für Innere Medizin, Universität zu Köln, Cologne, Germany.
authors.forename: D
authors.initials: D
authors.lastname: Müller-Wieland
authors.forename: B
authors.initials: B
authors.lastname: Behnke
authors.forename: D
authors.initials: D
authors.lastname: Diederichsen
authors.forename: W
authors.initials: W
authors.lastname: Krone
mesh_terms: D058668:Adrenergic alpha-1 Receptor Antagonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D058671:Adrenergic beta-1 Receptor Antagonists; D058672:Adrenergic beta-2 Receptor Antagonists; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D005227:Fatty Acids / Q000096:biosynthesis*; D006801:Humans; D066298:In Vitro Techniques; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism*; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects*; D018340:Receptors, Adrenergic, alpha-1 / Q000187:drug effects; D018341:Receptors, Adrenergic, alpha-2 / Q000187:drug effects; D011943:Receptors, Adrenergic, beta / Q000187:drug effects*; D018342:Receptors, Adrenergic, beta-1 / Q000187:drug effects; D018343:Receptors, Adrenergic, beta-2 / Q000187:drug effects
chemical_list: D058668:Adrenergic alpha-1 Receptor Antagonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D058671:Adrenergic beta-1 Receptor Antagonists; D058672:Adrenergic beta-2 Receptor Antagonists; D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D005227:Fatty Acids; D011942:Receptors, Adrenergic, alpha; D018340:Receptors, Adrenergic, alpha-1; D018341:Receptors, Adrenergic, alpha-2; D011943:Receptors, Adrenergic, beta; D018342:Receptors, Adrenergic, beta-1; D018343:Receptors, Adrenergic, beta-2