alexa G-proteins and beta-adrenergic stimulation of adenylate cyclase activity in the diabetic rat prostate.
Diabetes & Endocrinology

Diabetes & Endocrinology

Endocrinology & Metabolic Syndrome

Author(s): Carmena MJ, Clemente C, Carrero I, Solano RM, Prieto JC

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Abstract BACKGROUND: The consequences of experimental diabetes on membrane lipids, beta-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 (alpha s) and inhibitory (alpha i) 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 alpha s, alpha i1/2, and alpha i3/0 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 beta-adrenergic response of adenylate cyclase, as supported by previous data on the low density of beta-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.
This article was published in Prostate and referenced in Endocrinology & Metabolic Syndrome

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