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Isolated mouse islets respond to glucose with an initial peak of glucagon release followed by pulses of insulin and somatostatin in antisynchrony with glucagon

Hellman, Bo; Salehi, S Albert LU ; Grapengiesser, Eva and Gylfe, Erik (2012) In Biochemical and Biophysical Research Communications 417(4). p.1219-1223
Abstract
Recent studies of isolated human islets have shown that glucose induces hormone release with repetitive pulses of insulin and somatostatin in antisynchrony with those of glucagon. Since the mouse is the most important animal model we studied the temporal relation between hormones released from mouse islets. Batches of 5-10 islets were perifused and the hormones measured with radioimmunoassay in 30 s fractions. At 3 mM glucose, hormone secretion was stable with no detectable pulses of glucagon, insulin or somatostatin. Increase of glucose to 20 mM resulted in an early secretory phase with a glucagon peak followed by peaks of insulin and somatostatin. Subsequent hormone secretion was pulsatile with a periodicity of 5 min. Cross-correlation... (More)
Recent studies of isolated human islets have shown that glucose induces hormone release with repetitive pulses of insulin and somatostatin in antisynchrony with those of glucagon. Since the mouse is the most important animal model we studied the temporal relation between hormones released from mouse islets. Batches of 5-10 islets were perifused and the hormones measured with radioimmunoassay in 30 s fractions. At 3 mM glucose, hormone secretion was stable with no detectable pulses of glucagon, insulin or somatostatin. Increase of glucose to 20 mM resulted in an early secretory phase with a glucagon peak followed by peaks of insulin and somatostatin. Subsequent hormone secretion was pulsatile with a periodicity of 5 min. Cross-correlation analyses showed that the glucagon pulses were antisynchronous to those of insulin and somatostatin. In contrast to the marked stimulation of insulin and somatostatin secretion, the pulsatility resulted in inhibition of overall glucagon release. The cytoarchitecture of mouse islets differs from that of human islets, which may affect the interactions between the hormone-producing cells. Although indicating that paracrine regulation is important for the characteristic patterns of pulsatile hormone secretion, the mouse data mimic those of human islets with more than 20-fold variations of the insulin/glucagon ratio. The data indicate that the mouse serves as an appropriate animal model for studying the temporal relation between the islet hormones controlling glucose production in the liver. (C) 2012 Elsevier Inc. All rights reserved. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Insulin, Glucagon, Somatostatin, Islets, Pulsatile secretion, Antisynchrony
in
Biochemical and Biophysical Research Communications
volume
417
issue
4
pages
1219 - 1223
publisher
Elsevier
external identifiers
  • wos:000300196100019
  • scopus:84856299079
ISSN
1090-2104
DOI
10.1016/j.bbrc.2011.12.113
language
English
LU publication?
yes
id
4c950b5f-6ff0-40c8-9128-279364b5a9ad (old id 2409958)
date added to LUP
2012-04-02 09:32:45
date last changed
2017-08-20 04:04:09
@article{4c950b5f-6ff0-40c8-9128-279364b5a9ad,
  abstract     = {Recent studies of isolated human islets have shown that glucose induces hormone release with repetitive pulses of insulin and somatostatin in antisynchrony with those of glucagon. Since the mouse is the most important animal model we studied the temporal relation between hormones released from mouse islets. Batches of 5-10 islets were perifused and the hormones measured with radioimmunoassay in 30 s fractions. At 3 mM glucose, hormone secretion was stable with no detectable pulses of glucagon, insulin or somatostatin. Increase of glucose to 20 mM resulted in an early secretory phase with a glucagon peak followed by peaks of insulin and somatostatin. Subsequent hormone secretion was pulsatile with a periodicity of 5 min. Cross-correlation analyses showed that the glucagon pulses were antisynchronous to those of insulin and somatostatin. In contrast to the marked stimulation of insulin and somatostatin secretion, the pulsatility resulted in inhibition of overall glucagon release. The cytoarchitecture of mouse islets differs from that of human islets, which may affect the interactions between the hormone-producing cells. Although indicating that paracrine regulation is important for the characteristic patterns of pulsatile hormone secretion, the mouse data mimic those of human islets with more than 20-fold variations of the insulin/glucagon ratio. The data indicate that the mouse serves as an appropriate animal model for studying the temporal relation between the islet hormones controlling glucose production in the liver. (C) 2012 Elsevier Inc. All rights reserved.},
  author       = {Hellman, Bo and Salehi, S Albert and Grapengiesser, Eva and Gylfe, Erik},
  issn         = {1090-2104},
  keyword      = {Insulin,Glucagon,Somatostatin,Islets,Pulsatile secretion,Antisynchrony},
  language     = {eng},
  number       = {4},
  pages        = {1219--1223},
  publisher    = {Elsevier},
  series       = {Biochemical and Biophysical Research Communications},
  title        = {Isolated mouse islets respond to glucose with an initial peak of glucagon release followed by pulses of insulin and somatostatin in antisynchrony with glucagon},
  url          = {http://dx.doi.org/10.1016/j.bbrc.2011.12.113},
  volume       = {417},
  year         = {2012},
}