Autonomic nervous control of the endocrine secretion from the isolated, perfused pig pancreas

Holst, Jens J.; Schwartz, Thue W.; Sl, Jensen; Ov, Nielsen

doi:10.1016/0165-1838(86)90045-7

Cited by 57 publications

(40 citation statements)

References 20 publications

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“…The mechanism could not be related to disturbed insulin action since all patients, with or without neuropathy, were C-peptide negative. These observations may therefore be consistent with a role for the autonomic nervous system in the control of glucagon secretion [36,37]. Previous work in rodents showed that vagotomy [38] as well as ventromedial hypothalamic lesions [39] hampers the regulation of glucagon secretion following …”

Section: Discussionsupporting

confidence: 76%

“…A 80% reduction in the number of nerve endings in direct contact with alpha-cells was noted type 1 diabetes BB rats [41] which could be responsible for an impaired glucagon regulation as well as reduced PP secretion. However, acetylcholine activates glucagon secretion from isolated pancreatic alpha cells [42,43], indicating that glucagonostatic effect of acetylcholine on the whole pancreas is due to a more complex mechanism, perhaps involving inhibition of somatostatin secretion [37,44]. Our data are in agreement with this conclusion since the plasma glucagon to PP concentration ratio increased during the meal test in AN+ patients while it remained low and steady under control in AN-patients.…”

Section: Neuropathy Hamperssupporting

confidence: 82%

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Autonomic Diabetic Neuropathy Impairs Glucose and Dipeptidyl Peptidase 4 Inhibitor-Regulated Glucagon Concentration in Type 1 Diabetic Patients

et al. 2015

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Section: Discussionsupporting

confidence: 76%

Section: Neuropathy Hamperssupporting

confidence: 82%

Autonomic Diabetic Neuropathy Impairs Glucose and Dipeptidyl Peptidase 4 Inhibitor-Regulated Glucagon Concentration in Type 1 Diabetic Patients

et al. 2015

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“…Brain serotonergic changes are reported to regulate autonomic nerve function in rats [24]. The 5-HT content was increased in the cerebral cortex and brain stem during active pancreatic regeneration.…”

Section: Discussionmentioning

confidence: 99%

Decreased 5-HT2C receptor binding in the cerebral cortex and brain stem during pancreatic regeneration in rats

2005

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The purpose of this study was to investigate the role of central 5-HT2C receptor binding in rat model of pancreatic regeneration using 60-70% pancreatectomy. The 5-HT and 5-HT2c receptor kinetics were studied in cerebral cortex and brain stem of sham operated, 72 h pancreatectomised and 7 days pancreatectomised rats. Scatchard analysis with [3H] mesulergine in cerebral cortex showed a significant decrease (p < 0.05) in maximal binding (B^,ax) without any change in Kd in 72 h pancreatectomised rats compared with sham. The decreased Bmax reversed to sham level by 7 days after pancreatectomy. In brain stem , Scatchard analysis showed a significant decrease (p < 0.01) in Bax with a significant increase (p < 0.01) in Kd. Competition analysis in brain stem showed a shift in affinity towards a low affinity. These parameters were reversed to sham level by 7 days after pancreatectomy. Thus the results suggest that 5-HT through the 5-HT2C receptor in the brain has a functional regulatory role in the pancreatic regeneration. (Mol Cell Biochem 272: 165-170, 2005)

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“…Galantamine has previously been shown to exert antiinflammatory effects through brain-mediated and vagus nerve-dependent signaling (35,51). The vagus nerve innervates the pancreas, and vagus nerve cholinergic output controls pancreatic endocrine and exocrine secretion (60)(61)(62). A role for the vagus nerve has also been shown in suppressing pancreatic inflammation; surgical transection of the vagus nerve (vagotomy) results in exacerbated murine pancreatitis, thus indicating a tonic antiinflammatory role of these innervations (63).…”

Section: Discussionmentioning

confidence: 99%

Galantamine Attenuates Type 1 Diabetes and Inhibits Anti-Insulin Antibodies in Nonobese Diabetic Mice

Hanes

Olofsson

Kwan

et al. 2015

Mol Med

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Type 1 diabetes in mice is characterized by autoimmune destruction of insulin-producing pancreatic β-cells. Disease pathogenesis involves invasion of pancreatic islets by immune cells, including macrophages and T cells, and production of antibodies to self-antigens, including insulin. Activation of the inflammatory reflex, the neural circuit that inhibits inflammation, culminates on cholinergic receptor signals on immune cells to attenuate cytokine release and inhibit B-cell antibody production. Here, we show that galantamine, a centrally acting acetylcholinesterase inhibitor and an activator of the inflammatory reflex, attenuates murine experimental type 1 diabetes. Administration of galantamine to animals immunized with keyhole limpet hemocyanin (KLH) significantly suppressed splenocyte release of immunoglobulin G (IgG) and interleukin (IL)-4 and IL-6 during KLH challenge ex vivo. Administration of galantamine beginning at 1 month of age in nonobese diabetic (NOD) mice significantly delayed the onset of hyperglycemia, attenuated immune cell infiltration in pancreatic islets and decreased anti-insulin antibodies in serum. These observations indicate that galantamine attenuates experimental type 1 diabetes in mice and suggest that activation of the inflammatory reflex should be further studied as a potential therapeutic approach.

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Autonomic nervous control of the endocrine secretion from the isolated, perfused pig pancreas

Cited by 57 publications

References 20 publications

Autonomic Diabetic Neuropathy Impairs Glucose and Dipeptidyl Peptidase 4 Inhibitor-Regulated Glucagon Concentration in Type 1 Diabetic Patients

Autonomic Diabetic Neuropathy Impairs Glucose and Dipeptidyl Peptidase 4 Inhibitor-Regulated Glucagon Concentration in Type 1 Diabetic Patients

Decreased 5-HT2C receptor binding in the cerebral cortex and brain stem during pancreatic regeneration in rats

Galantamine Attenuates Type 1 Diabetes and Inhibits Anti-Insulin Antibodies in Nonobese Diabetic Mice

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