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

✍ Scribed by Carmena, María J.; Clemente, Celia; Carrero, Isabel; Solano, Rosa M.; Prieto, Juan C.

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 577 KB
• Volume: 33
• Category: Article
• ISSN: 0270-4137
• DOI: 10.1002/(sici)1097-0045(19970915)33:1<46::aid-pros8>3.0.co;2-7

✦ Synopsis

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.