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Glucose Induces Glucagon Release Pulses Antisynchronous with Insulin and Sensitive to Purinoceptor Inhibition.

Grapengiesser, Eva ; Salehi, S Albert LU orcid ; Qader, Saleem LU and Hellman, Bo (2006) In Endocrinology 147(2006 Apr 13). p.3472-3477
Abstract
Both increase of the glucose concentration and activation of purinoceptors are known to affect pancreatic alpha-cells. Effects obtained with various purino derivatives at 2.8 and 8.3 mmol/ liter glucose have been taken to indicate that external ATP is less potent than adenosine as a stimulator of glucagon release. However, when making a corresponding comparison at 20 mmol/ liter glucose, we observed marked stimulation of glucagon release from isolated rat islets with 100 mu mol/liter adenosine-5- O-2-thiodiphosphate but inhibition with 10 mu mol/liter adenosine. Analyses of 30-sec samples of perfusate from rat pancreas indicated that a rise of the glucose concentration from 3 to 20 mmol/ liter rapidly induces a glucagon peak followed by... (More)
Both increase of the glucose concentration and activation of purinoceptors are known to affect pancreatic alpha-cells. Effects obtained with various purino derivatives at 2.8 and 8.3 mmol/ liter glucose have been taken to indicate that external ATP is less potent than adenosine as a stimulator of glucagon release. However, when making a corresponding comparison at 20 mmol/ liter glucose, we observed marked stimulation of glucagon release from isolated rat islets with 100 mu mol/liter adenosine-5- O-2-thiodiphosphate but inhibition with 10 mu mol/liter adenosine. Analyses of 30-sec samples of perfusate from rat pancreas indicated that a rise of the glucose concentration from 3 to 20 mmol/ liter rapidly induces a glucagon peak followed by regular 4- to 5-min pulses. The glucagon pulses preceded those of insulin with a phase shift (1.8 +/- 0.1 min) near half the interpeak interval. Because of the antisynchrony, the maximal glucagon effect on liver cells will be manifested during periods with low concentrations of insulin. In support for the idea that neural P2Y(1) receptors are important for coordinating the secretory activity of the islets, both the insulin and glucagon pulses disappeared in the presence of the purinoceptor inhibitor MRS 2179 (10 mu mol/liter). However, in contrast to what was observed for insulin, MRS 2179 lowered average glucagon release to the level of the oscillatory nadirs. (Less)
Please use this url to cite or link to this publication:
author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Endocrinology
volume
147
issue
2006 Apr 13
pages
3472 - 3477
publisher
Oxford University Press
external identifiers
  • wos:000238312400036
  • pmid:16614082
  • scopus:33745165968
  • pmid:16614082
ISSN
0013-7227
DOI
10.1210/en.2005-1431
language
English
LU publication?
yes
id
b6f6291b-936b-44ba-91b6-bd57f9d9e12a (old id 155906)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16614082&dopt=Abstract
date added to LUP
2016-04-01 12:13:57
date last changed
2021-02-17 07:37:36
@article{b6f6291b-936b-44ba-91b6-bd57f9d9e12a,
  abstract     = {Both increase of the glucose concentration and activation of purinoceptors are known to affect pancreatic alpha-cells. Effects obtained with various purino derivatives at 2.8 and 8.3 mmol/ liter glucose have been taken to indicate that external ATP is less potent than adenosine as a stimulator of glucagon release. However, when making a corresponding comparison at 20 mmol/ liter glucose, we observed marked stimulation of glucagon release from isolated rat islets with 100 mu mol/liter adenosine-5- O-2-thiodiphosphate but inhibition with 10 mu mol/liter adenosine. Analyses of 30-sec samples of perfusate from rat pancreas indicated that a rise of the glucose concentration from 3 to 20 mmol/ liter rapidly induces a glucagon peak followed by regular 4- to 5-min pulses. The glucagon pulses preceded those of insulin with a phase shift (1.8 +/- 0.1 min) near half the interpeak interval. Because of the antisynchrony, the maximal glucagon effect on liver cells will be manifested during periods with low concentrations of insulin. In support for the idea that neural P2Y(1) receptors are important for coordinating the secretory activity of the islets, both the insulin and glucagon pulses disappeared in the presence of the purinoceptor inhibitor MRS 2179 (10 mu mol/liter). However, in contrast to what was observed for insulin, MRS 2179 lowered average glucagon release to the level of the oscillatory nadirs.},
  author       = {Grapengiesser, Eva and Salehi, S Albert and Qader, Saleem and Hellman, Bo},
  issn         = {0013-7227},
  language     = {eng},
  number       = {2006 Apr 13},
  pages        = {3472--3477},
  publisher    = {Oxford University Press},
  series       = {Endocrinology},
  title        = {Glucose Induces Glucagon Release Pulses Antisynchronous with Insulin and Sensitive to Purinoceptor Inhibition.},
  url          = {http://dx.doi.org/10.1210/en.2005-1431},
  doi          = {10.1210/en.2005-1431},
  volume       = {147},
  year         = {2006},
}