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Neuronostatin inhibits glucose-stimulated insulin secretion via direct action on the pancreatic [alpha]-cell

Neuronostatin is a recently described peptide hormone encoded by the somatostatin gene. We previously showed that intraperitoneal injection of neuronostatin into mice resulted in c-Jun accumulation in pancreatic islets in a pattern consistent with the activation of glucagon-producing ...-cells. We t...

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Bibliographic Details
Published in:American journal of physiology: endocrinology and metabolism 2014-06, Vol.306 (11), p.E1257
Main Authors: Salvatori, Alison S, Elrick, Mollisa M, Samson, Willis K, Corbett, John A, Yosten, Gina LC
Format: Article
Language:English
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Summary:Neuronostatin is a recently described peptide hormone encoded by the somatostatin gene. We previously showed that intraperitoneal injection of neuronostatin into mice resulted in c-Jun accumulation in pancreatic islets in a pattern consistent with the activation of glucagon-producing ...-cells. We therefore hypothesized that neuronostatin could influence glucose homeostasis via a direct effect on the ...-cell. Neuronostatin enhanced low-glucose-induced glucagon release in isolated rat islets and in the immortalized ...-cell line ...TC1-9. Furthermore, incubation with neuronostatin led to an increase in transcription of glucagon mRNA, as determined by RT-PCR. Neuronostatin also inhibited glucose-stimulated insulin secretion from isolated islets. However, neuronostatin did not alter insulin release from the ...-cell line INS 832/13, indicating that the effect of neuronostatin on insulin secretion may be secondary to a direct action on the ...-cell. In agreement with our in vitro data, intra-arterial infusion of neuronostatin in male rats delayed glucose disposal and inhibited insulin release during a glucose challenge. These studies suggest that neuronostatin participates in maintaining glucose homeostasis through cell-cell interactions between ...-cells and ...-cells in the endocrine pancreas, leading to attenuation in insulin secretion. (ProQuest: ... denotes formulae/symbols omitted.)
ISSN:0193-1849
1522-1555