Neonatal capsaicin-treatment in mice: effects on pancreatic peptidergic nerves and 2-deoxy-D-glucose-induced insulin and glucagon secretion.

@article{Karlsson1992NeonatalCI,
  title={Neonatal capsaicin-treatment in mice: effects on pancreatic peptidergic nerves and 2-deoxy-D-glucose-induced insulin and glucagon secretion.},
  author={Sven Karlsson and Frank Sundler and Bo Ahr{\'e}n},
  journal={Journal of the autonomic nervous system},
  year={1992},
  volume={39 1},
  pages={
          51-9
        }
}

University of Groningen Ablation of capsaicin-sensitive afferent nerves affects insulin response during an intravenous glucose tolerance test

It is hypothesized that sensory afferents could play a role in the aetiology of pathologies where glucohomeostatic mechanisms are disturbed, as is in type 2 diabetes mellitus, and it is suggested that capsaicin-sensitive nerves could be involved in the regulation of insulin sensitivity.

Involvement of capsaicin-sensitive nerves in regulating the hormone and glucose metabolic response to endotoxin.

Data indicate that sensory afferent neurons play a critical role in the early secretory response of glucagon and catecholamines, the maintenance of tissuecatecholamine responsiveness, and the stimulation of glucose production after LPS.

The role of CGRP and afferent nerves in the modulation of pancreatic enzyme secretion in the rat

  • J. JaworekS. KonturekA. Szlachcic
  • Biology, Medicine
    International journal of pancreatology : official journal of the International Association of Pancreatology
  • 1997
Stimulation of pancreatic sensory nerves by capsaicin produced secretory effects probably caused, at least in part, by the release of CGRP, which increased enzyme secretion, and this secretion was abolished by previous inactivation of sensory nerve by this neurotoxin.

Insulin secretion by gastrin-releasing peptide in mice: ganglionic versus direct islet effect.

It is concluded that the insulinotropic effect of GRP in the mouse is mediated by both direct islet effects and through activation, at the ganglionic level, of postganglionic cholinergic nerves.

Insulin secretion by gastrin-releasing peptide in mice: ganglionic versus direct islet effect.

It is concluded that the insulinotropic effect of GRP in the mouse is mediated by both direct islet effects and through activation, at the ganglionic level, of postganglionic cholinergic nerves.

Pancreatic endocrine responses to substance P and calcitonin gene-related peptide in conscious calves.

The results suggest that SP and CGRP may modulate the secretion of PP and glucagon in the normal conscious calf but not that of insulin, and it is also possible that SP modulates secretion of pancreatic glucagons in these animals.

Sensory nerve inactivation by resiniferatoxin improves insulin sensitivity in male obese Zucker rats.

RTX treatment and, hence, sensory nerve desensitization of adult male obese Zucker rats improved oral glucose tolerance by enhancing insulin secretion, and, in particular, by improving insulin sensitivity.

References

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Effect of capsaicin‐sensitive sensory nerves on plasma glucose and catecholamine levels during 2‐deoxyglucose‐induced stress in conscious rats

The results indicate that capsaicin‐sensitive sensory fibres are not required to maintain adrenal CA secretion during glucopenic stress in the conscious rat but are required for maintenance of blood glucose levels.

Capsaicin-sensitive nerves are required for glucostasis but not for catecholamine output during hypoglycemia in rats.

Somaostatin and SMS-(201-995), a somatostatin analogue, both potentiated and prolonged the insulin-induced hypoglycemia, resulting in an increase in circulating CA levels that was suppressed by hexamethonium and atropine.

Calcitonin gene-related peptide: occurrence in pancreatic islets in the mouse and the rat and inhibition of insulin secretion in the mouse.

It is concluded that CGRP occurs in islet cells and in intrapancreatic nerve fibers of both the mouse and the rat, and inhibits both basal and stimulated insulin secretion in vivo in the mouse.

Stimulation of pancreatic polypeptide and glucagon secretion by 2-deoxy-D-glucose in man: evidence for cholinergic mediation.

The data demonstrate that 2-DG induces a powerful stimulation of hPP secretion in normal subjects and suggest that this action is mediated in part, if not entirely, by the parasympathetic nervous system and seems also to be dependent on cholinergic transmission.

The relative importance of nervous system and hormones to the 2-deoxy-D-glucose-induced hyperglycemia in fed rats.

The results suggest that there are three distinct sympathetic nervous system responses to 2-DG-induced central nervous system-mediated hyperglycemia, which is not dependent on only one of those three systems, it is dependent on all of them.

Galanin release during pancreatic nerve stimulation is sufficient to influence islet function.

The effect of MPNS on IRI, SLI, and IRG output was compared with the effect of synthetic galanin infused directly into the pancreatic artery at a rate that reproduced the MPNS-induced spillover of GLIR, which was nearly identical to the increment produced by MPNS.

The mechanism of 2-deoxy-glucose-induced insulin secretion in the mouse.

2-deoxy-glucose induces a stimulation of insulin secretion in vivo in the mouse predominantly by a cholinergic mechanism, which activates alpha-adrenoceptor mechanisms which affect the size of the insulin secretory response.