Effects of streptozocin-induced diabetes on sympathetic and parasympathetic stimulation of parotid salivary gland function in rats

Anderson, L. C.; Garrett, J. R.; Thulin, A.; Proctor, G. B.

doi:10.2337/diabetes.38.11.1381

Cited by 14 publications

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“…However, water-restriction induced a remarkable decrease in salivary secretion of the STZ rats compared with the control. On the other hand, pilocarpine-stimulated whole saliva secretion was remarkably decreased in STZ rats, compared to the control rats, as well as those reported by other investigators (15,23,24). The volume of saliva elicited by the parotid gland was also decreased after stimulation of pilocarpine and its level was about 30% of the control level (Fig.…”

Section: Discussionsupporting

confidence: 75%

Lowered Susceptibility of Muscarinic Receptor Involved in Salivary Secretion of Streptozotocin-Induced Diabetic Rats

Watanabe

Yamagishi-Wang

Kawaguchi

2001

Japanese Journal of Pharmacology

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ABSTRACT-We investigated the responses of salivary secretion and the susceptibility of the muscarinic receptors in the salivary glands of the streptozotocin (STZ)-induced diabetic rats (STZ rats). Giving water ad libitum, the amount of whole saliva with no stimulation was similar in the STZ and the control rats. Pilocarpine increased salivary secretion in both groups, although the effect in the STZ rats was two to three fold less than in the control rats. If the animals were restricted from taking water for 6 h, salivary secretion was not slightly changed in the STZ rats in spite of a remarkable increase in the control. An obvious decrease in salivary secretion of the STZ rats was negatively correlated with an increase in urination. Furthermore, salivary secretion from the parotid gland was increased in a dose-dependent manner with pilocarpine in the control rats, but not in the STZ rats. In the [3 H]quinuclidinyl benzilate (QNB) binding studies for muscarinic receptor of the STZ rats, Bmax was decreased in the parotid gland and Kd was increased in the submandibular gland. Competitive inhibition of [3 H]QNB binding to both glands showed an increase in IC50 of pilocarpine and carbachol. These results suggest that a decrease in salivary secretion of STZ rats is not only induced by a water loss, but also closely associated with the lowered susceptibility of the muscarinic receptors.

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Section: Discussionsupporting

confidence: 75%

Lowered Susceptibility of Muscarinic Receptor Involved in Salivary Secretion of Streptozotocin-Induced Diabetic Rats

Watanabe

Yamagishi-Wang

Kawaguchi

2001

Japanese Journal of Pharmacology

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“…Reduction in both sensitivity to norepinephrine and availability of norepinephrine was observed only 2 weeks after the induction of diabetes with streptozotocin [20]. Furthermore, when autonomic neuropathy is present, the responses of the pa- [16] and the vas deferens [21] to sympathetic or noradrenergic nerve stimulation are reported to be reduced. Accordingly the decreased glucagon response to SNS at the low glucose concentration in the diabetic rats may be related to defects in the sympathetic nervous system and decreased Alpha-cell sensitivity to norepinephrine.…”

Section: Discussionmentioning

confidence: 99%

“…Other possible contributing factors are diabetic autonomic neuropathy or an alteration in catecholamine sensitivity of diabetic Alpha cells. Schmidt et al [15] and Anderson et al [16], however, have reported that they T. Kurose et al: S3~npathetic nerve and islet hormones in diabetes failed to demonstrate axonal dystrophy of the autonomic nerves, a characteristic of diabetic neuropathy, in animals diabetic for 4 months or less, in marked contrast to the presence of axonopathy of the somatic nerves observed as early as 4 weeks after diabetes is induced [17]. Diabetic Alpha-ceil sensitivity to catecholamines has been reported to be unchanged in NSZ rats [18] and in rats treated acutely with streptozotocin [19].…”

Section: Discussionmentioning

confidence: 99%

Glucagon, insulin and somatostatin secretion in response to sympathetic neural activation in streptozotocin-induced diabetic rats. A study with the isolated perfused rat pancreas in vitro

et al. 1992

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Summary. Changes in glucagon, insulin and somatostatin secretion induced by electrical splanchnic nerve stimulation were examined in rats treated with streptozotocin as neonates and as adults. In order to study the direct neural effects we used the isolated perfused rat pancreas with intact left splanchnic nerve in vitro. In normal rats splanchnic nerve stimulation causes significant decreases in insulin (30-40%) and somatostatin (30-50%) secretion at both 16.7 mmol/1 and 1 mmol/1 glucose concentrations. In the neonatal streptozotocin-diabetic rats splanchnic nerve stimulation at 16.7 mmol/1 glucose decreased insulin secretion (14%) further than in the control rats (30%), however, somatostatin secretion did not decrease to the same extent. Similar results were also observed at the low (1 mmol/1) glucose concentration. On the other hand, percent decreases of insulin and somatostatin secretion induced by splanchnic nerve stimulation in the streptozotocin-diabetic rats were similar to the values observed in the normal control rats. The glucagon secretion in response to splanchnic nerve stimulation at 16.7mmoi/I glucose from pancreatic Alpha ceils in both types of induced diabetes is exaggerated, and the degree of exaggeration seems to parallel the severity of the hyperglycaemia. However, the splanchnic nerve stimulation-induced glucagon secretion at 1 mmol/1 glucose was impaired in the streptozotocin-diabetic rats, but not in the neonatal streptozotocin-diabetic rats. These data suggest that the sensitivity of diabetic Alpha and Delta cells to sympathetic neural activation are blunted, whereas the sensitivity of Beta cells is enhanced in the diabetic animal model. Key words:Glucagon, insulin, somatostatin, streptozotocin, sympathetic nerve, diabetic rat.It has been reported that various clinical stress states are associated with catecholamine excess and hyperglycaemia, resulting in impaired insulin secretion and hyperglucagonaemia [1,2]. Furthermore, exaggerated glucagon responses to epinephrine have been observed in diabetic patients [2], and this exaggeration of glucagon secretion may have clinical importance in the pathogenesis of diabetes mellitus [3]. On the other hand, pancreatic Alpha-cell responses to changes in glucose concentrations are also abnormal in diabetes [4].Portha et al. [5] and Weir et al. [6] have reported independently that rats receiving streptozotocin during the neonatal period show a resemblance to human Type 2 (non-insulin-dependent) diabetes with a mild diabetic state showing selective insensitivity to glucose in Beta cells, while insulin secretion in response to other secretagogues is preserved. Furthermore, adult rats receiving streptozotocin develop severe insulin deficiency, and are considered to be one of the models of Type 1 (insulin-dependent) diabetes [7].In the present study we have investigated the effect of sympathetic neural activation on the endocrine pancreas in the animal models of diabetes. Furthermore, in order to elucidate the mechanism of abnormal glucagon secretion fro...

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“…Furthermore, in both strains, diabetes reduced the sympathetic nerve activity. Morphological damage to the sympathetic innervation of salivary glands in diabetic rats includes fiber degeneration (5,16) and decreased number and size of fibers (41) as well as focal dilatations of axons and accumulation of subcellular organelles. Additionally, reduced noradrenaline content and release in sympathetic neurons of salivary glands has been described in diabetic rats (40).…”

Section: Discussionmentioning

confidence: 99%

SGLT1 protein expression in plasma membrane of acinar cells correlates with the sympathetic outflow to salivary glands in diabetic and hypertensive rats

Sabino-Silva

Alves-Wagner

Burgi

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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Salivary gland dysfunction is a feature in diabetes and hypertension. We hypothesized that sodium-glucose cotransporter 1 (SGLT1) participates in salivary dysfunctions through a sympathetic- and protein kinase A (PKA)-mediated pathway. In Wistar-Kyoto (WKY), diabetic WKY (WKY-D), spontaneously hypertensive (SHR), and diabetic SHR (SHR-D) rats, PKA/SGLT1 proteins were analyzed in parotid and submandibular glands, and the sympathetic nerve activity (SNA) to the glands was monitored. Basal SNA was threefold higher in SHR ( P < 0.001 vs. WKY), and diabetes decreased this activity (∼50%, P < 0.05) in both WKY and SHR. The catalytic subunit of PKA and the plasma membrane SGLT1 content in acinar cells were regulated in parallel to the SNA. Electrical stimulation of the sympathetic branch to salivary glands increased (∼30%, P < 0.05) PKA and SGLT1 expression. Immunohistochemical analysis confirmed the observed regulations of SGLT1, revealing its location in basolateral membrane of acinar cells. Taken together, our results show highly coordinated regulation of sympathetic activity upon PKA activity and plasma membrane SGLT1 content in salivary glands. Furthermore, the present findings show that diabetic- and/or hypertensive-induced changes in the sympathetic activity correlate with changes in SGLT1 expression in basolateral membrane of acinar cells, which can participate in the salivary glands dysfunctions reported by patients with these pathologies.

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Effects of streptozocin-induced diabetes on sympathetic and parasympathetic stimulation of parotid salivary gland function in rats

Cited by 14 publications

References 0 publications

Lowered Susceptibility of Muscarinic Receptor Involved in Salivary Secretion of Streptozotocin-Induced Diabetic Rats

Lowered Susceptibility of Muscarinic Receptor Involved in Salivary Secretion of Streptozotocin-Induced Diabetic Rats

Glucagon, insulin and somatostatin secretion in response to sympathetic neural activation in streptozotocin-induced diabetic rats. A study with the isolated perfused rat pancreas in vitro

SGLT1 protein expression in plasma membrane of acinar cells correlates with the sympathetic outflow to salivary glands in diabetic and hypertensive rats

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