THE EFFECTS OF STREPTOZOTOCIN-INDUCED DIABETES ON NOREPINEPHRINE AND CHOLINERGIC ENZYME-ACTIVITIES IN RAT PAROTID AND SUBMANDIBULAR GLANDS

Citation
Lc. Anderson et Jr. Garrett, THE EFFECTS OF STREPTOZOTOCIN-INDUCED DIABETES ON NOREPINEPHRINE AND CHOLINERGIC ENZYME-ACTIVITIES IN RAT PAROTID AND SUBMANDIBULAR GLANDS, Archives of oral biology, 39(2), 1994, pp. 91-97
Citations number
41
Categorie Soggetti
Dentistry,Oral Surgery & Medicine
Journal title
ISSN journal
00039969
Volume
39
Issue
2
Year of publication
1994
Pages
91 - 97
Database
ISI
SICI code
0003-9969(1994)39:2<91:TEOSDO>2.0.ZU;2-R
Abstract
Autonomic neuropathy is a common complication of diabetes mellitus, an d both morphological and physiological data suggest that salivary glan d function in diabetic rats is affected by neuropathies involving symp athetic and parasympathetic nerves. Therefore, glandular levels of the adrenergic neurotransmitter, norepinephrine (NE) and two cholinergic enzymes, choline acetyltransferase (ChAT) and acetylcholinesterase (AC hE), were investigated in 6-month streptozotocin-diabetic rats. Signif icant, but variable, increases in total parotid NE (ng/gland) were obs erved in diabetic rats, whereas total submandibular NE was lower in di abetic animals than in controls. However, on a ng/mg tissue basis, NE levels in both the parotid gland, and less dramatically, in the subman dibular gland were increased. Somewhat different results were observed for AChE and ChAT. AChE was marginally greater in the parotid glands of diabetic rats, whereas AChE and ChAT levels were significantly lowe r in diabetic than control submandibular glands. Expressed as enzymati c activity per mg tissue, submandibular gland ChAT, but not AChE, was increased. Short-term (3-day) insulin treatment of diabetic animals ha d no significant effects on total NE, AChE or ChAT in the parotid glan d, but led to a further reduction in submandibular ChAT. With regard t o function, changes in AChE appeared to be correlated with previously reported morphological assessments of parotid gland innervation in dia betic animals. Thus, the decreased response of the parotid gland in di abetic rats to parasympathetic stimulation may be related in part to t he increase in AChE.