A possible cyclic AMP-mediated regulation of microsomal fatty acyl-CoA desaturation system in Tetrahymena microsomes

Abstract

Profound alterations in the microsomal fatty acyl-CoA desaturase activities and cyclic AMP production of a unicellular eukaryote, Tetrahymena pyriformis NT-1, originally grown in the glucose-deficient medium, were observed, following the administration of glucose or β-adrenergic agonists such as epinephrine and isoproterenol. There was a great increase of stearoyl-CoA (Δ 8 desaturase activity coincident with a 2-fold decrease of oleoyl-CoA (Δ 12) desaturase activity over the first 2 h after administration of these compounds. During this period of time, it was found that the production in vivo of labeled oleic acid from [ 14C]acetic or [ 3H]palmitic acid increases 2-fold and the formation in vivo of each labeled linoleic and γ-linolenic acids drastically decreases. Glucose or β-adrenergic agonists caused an increase of stearoyl-CoA-stimulated reoxidation rate of NADH-reduced cytochrome b 5 but depressed oleoyl-CoA-stimulated reoxidation rate of b 5, indicating that both desaturase activities are controlled by the respective terminal components of the desaturase system. A significant and reproducible increase of adenylate cyclase activity and a slight decrease of cyclic AMP phosphodiesterase activity were observed to occur within the first 2 h after the addition of these compounds, when cyclic AMP content in Tetrahymena cell rose by 3–4-fold. Propranolol, a β-adrenergic blocker, abolished the effects of glucose or β-adrenergic agonists on the activities of fatty acyl-CoA desaturases and the terminal components as well as cyclic AMP production of cells. These results suggest that glucose and β-adrenergic agonists may modulate the microsomal fatty acyl-CoA desaturase system in Tetrahymena by acting through the increase of intracellular cyclic AMP content.