Premium
G‐proteins and β‐adrenergic stimulation of adenylate cyclase activity in the diabetic rat prostate
Author(s) -
Carmena María J.,
Clemente Celia,
Carrero Isabel,
Solano Rosa M.,
Prieto Juan C.
Publication year - 1997
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/(sici)1097-0045(19970915)33:1<46::aid-pros8>3.0.co;2-7
Subject(s) - endocrinology , medicine , adenylate kinase , cyclase , stimulation , forskolin , diabetes mellitus , adrenergic , streptozotocin , receptor , chemistry , biology
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 (α s ) and inhibitory (α i ) G‐protein subunits. Changes in membrane lipid composition were estimated by [1‐ 14 C] acetate incorporation into lipid subclasses. RESULTS The efficacy of isoproterenol on stimulation of adenylate cyclase activity and the levels of α s , α i1/2 , and α 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‐ 14 C] 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 G s and G i proteins levels and even of the enzyme itself in the diabetic rat prostate. Prostate 33:46–54, 1997. © 1997 Wiley‐Liss, Inc.