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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Am+J+Physiol+Endocrinol+Metab
2014 ; 306
(11
): E1257-63
Nephropedia Template TP
gab.com Text
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Twit Text #
English Wikipedia
Neuronostatin inhibits glucose-stimulated insulin secretion via direct action on
the pancreatic ?-cell
#MMPMID24735892
Salvatori AS
; Elrick MM
; Samson WK
; Corbett JA
; Yosten GL
Am J Physiol Endocrinol Metab
2014[Jun]; 306
(11
): E1257-63
PMID24735892
show ga
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.
|Animals
[MESH]
|Area Under Curve
[MESH]
|Blood Glucose/metabolism
[MESH]
|Blotting, Western
[MESH]
|Bradykinin/pharmacology
[MESH]
|Cell Line
[MESH]
|Cyclic AMP-Dependent Protein Kinases/metabolism
[MESH]