G‐proteins and β‐adrenergic stimulation of adenylate cyclase activity in the diabetic rat prostate

Abstract

BACKGROUND The consequences of experimental diabetes on membrane lipids, β-adrenergic stimulation of adenylate cyclase activity, and G-protein levels in the prostate gland are not defined. METHODS Prostatic membranes from control and streptozotocin (STZ)-diabetic rats were used to study adenylate cyclase stimulation as well as for immunodetection of stimulatory (αs) and inhibitory (αi) G-protein subunits. Changes in membrane lipid composition were estimated by [1-14C] acetate incorporation into lipid subclasses. RESULTS The efficacy of isoproterenol on stimulation of adenylate cyclase activity and the levels of αs, αi1/2, and αi3/0 G-protein subunits were drastically reduced in prostatic membranes from STZ-diabetic rats. Insulin treatment of diabetic rats tended to normalize G-protein levels, but it was ineffective on the poor adenylate cyclase response to isoproterenol or forskolin. However, it prevented enzyme desensitization to vasoactive intestinal peptide. The pattern of [1-14C] acetate incorporation into lipid subclasses did not vary with diabetes or insulin treatment. CONCLUSIONS STZ-induced diabetes results in desensitization for the β-adrenergic response of adenylate cyclase, as supported by previous data on the low density of β-adrenergic receptors and the present results on the general decrease of Gs and Gi proteins levels and even of the enzyme itself in the diabetic rat prostate. Prostate 33:46–54, 1997. © 1997 Wiley-Liss, Inc.