beta-adrenergic receptors and adenylate cyclase activity in the parotid acinar cells from acute streptozotocin-induced diabetic rats

Citation
T. Komabayashi et al., beta-adrenergic receptors and adenylate cyclase activity in the parotid acinar cells from acute streptozotocin-induced diabetic rats, RES COM M P, 107(3-4), 2000, pp. 311-322
Citations number
23
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
RESEARCH COMMUNICATIONS IN MOLECULAR PATHOLOGY AND PHARMACOLOGY
ISSN journal
10780297 → ACNP
Volume
107
Issue
3-4
Year of publication
2000
Pages
311 - 322
Database
ISI
SICI code
1078-0297(2000)107:3-4<311:BRAACA>2.0.ZU;2-M
Abstract
The changes in beta -adrenergic receptors and in adenylate cyclase (AC) act ivity were investigated in parotid glands from rats with acute diabetic mel litus (DM) induced by a single injection of streptozotocin (STZ, 80 mg/kg). The animals were divided into three groups: control rats, DM rats, and ins ulin-treated DM rats. Experiments were performed 7 days after the injection of STZ. Amylase and norepinephrine (NE) contents in parotid glands were ma rkedly decreased in DM rats in comparison with control rats. The density of beta -adrenergic receptor decreased in DM rats, but its affinity for ligan d was unaffected. The effect of GTP on isoprenaline (ISO)-stimulated adenyl ate cyclase (AC) activity significantly decreased in DM rats, but forskolin -stimulated AC activity was unaltered. In addition, diabetes induced the bl unted response of AC activity to ISO. The changes in AC activity and in amy lase content induced by diabetes were restored by insulin, but those in NE content and receptor density could not. These observations indicate that di abetes decreases NE and amylase contents, receptor density, and receptor-AC coupling in parotid gland, and that these changes would occur in the earli er stage of acute STZ-induced diabetic state.