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The apj receptor is expressed in pancreatic islets and its ligand, apelin, inhibits insulin secretion in mice.

Sörhede Winzell, Maria LU ; Magnusson, Caroline LU and Ahrén, Bo LU (2005) In Regulatory Peptides 131(1-3). p.12-17
Abstract
Apelin is the endogenous ligand of the G-protein coupled apj receptor. Apelin is expressed in the brain, the hypothalamus and the stomach and was recently shown also to be an adipokine secreted from the adipocytes. Although apelin has been suggested to be involved in the regulation of food intake, it is not known whether the peptide affects islet function and glucose homeostasis. We show here that the apj receptor is expressed in pancreatic islets and that intravenous administration of full-length apelin-36 (2 nmol/kg) inhibits the rapid insulin response to intravenous glucose (1 g/kg) by 35% in C57BL/6J mice. Thus, the acute (1-5 min) insulin response to intravenous glucose was 682 +/- 23 pmol/l after glucose alone (n = 17) and 445 +/- 58... (More)
Apelin is the endogenous ligand of the G-protein coupled apj receptor. Apelin is expressed in the brain, the hypothalamus and the stomach and was recently shown also to be an adipokine secreted from the adipocytes. Although apelin has been suggested to be involved in the regulation of food intake, it is not known whether the peptide affects islet function and glucose homeostasis. We show here that the apj receptor is expressed in pancreatic islets and that intravenous administration of full-length apelin-36 (2 nmol/kg) inhibits the rapid insulin response to intravenous glucose (1 g/kg) by 35% in C57BL/6J mice. Thus, the acute (1-5 min) insulin response to intravenous glucose was 682 +/- 23 pmol/l after glucose alone (n = 17) and 445 +/- 58 pmol/l after glucose plus apelin-36 (n = 18; P=0.017). This was associated with impaired glucose elimination (the 5-20 min glucose elimination was 2.9 +/- 0.1%/min after glucose alone versus 2.3 +/- 0.2%/min after glucose plus apelin-36, P=0.008). Apelin (2 nmol/kg) also inhibited the insulin response to intravenous glucose in obese insulin resistant high-fat fed C57BL/6J mice (P=0.041). After 60 min incubation of isolated islets from normal mice, insulin secretion in the presence of 16.7 mmol/l glucose was inhibited by apelin-36 at 1 pmol/l, whereas apelin-36 did not significantly affect insulin secretion at 2.8 or 8.3 mmol/l glucose or after stimulation of insulin secretion by KCI. Islet glucose oxidation at 16.7 mmol/l was not affected by apelin-36. We conclude that the apj receptor is expressed in pancreatic islets and that apelin-36 inhibits glucose-stimulated insulin secretion both in vivo and in vitro. This may suggest that the islet beta-cells are targets for apelin-36. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
apj receptor, islets, mice, insulin secretion, apelin
in
Regulatory Peptides
volume
131
issue
1-3
pages
12 - 17
publisher
Elsevier
external identifiers
  • wos:000232709100002
  • pmid:15970338
  • scopus:25844530179
ISSN
1873-1686
DOI
10.1016/j.regpep.2005.05.004
language
English
LU publication?
yes
id
9d2c1723-5217-42d8-b29c-036207a349f0 (old id 139874)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15970338&query_hl=164
date added to LUP
2007-07-10 14:27:49
date last changed
2017-10-01 03:55:36
@article{9d2c1723-5217-42d8-b29c-036207a349f0,
  abstract     = {Apelin is the endogenous ligand of the G-protein coupled apj receptor. Apelin is expressed in the brain, the hypothalamus and the stomach and was recently shown also to be an adipokine secreted from the adipocytes. Although apelin has been suggested to be involved in the regulation of food intake, it is not known whether the peptide affects islet function and glucose homeostasis. We show here that the apj receptor is expressed in pancreatic islets and that intravenous administration of full-length apelin-36 (2 nmol/kg) inhibits the rapid insulin response to intravenous glucose (1 g/kg) by 35% in C57BL/6J mice. Thus, the acute (1-5 min) insulin response to intravenous glucose was 682 +/- 23 pmol/l after glucose alone (n = 17) and 445 +/- 58 pmol/l after glucose plus apelin-36 (n = 18; P=0.017). This was associated with impaired glucose elimination (the 5-20 min glucose elimination was 2.9 +/- 0.1%/min after glucose alone versus 2.3 +/- 0.2%/min after glucose plus apelin-36, P=0.008). Apelin (2 nmol/kg) also inhibited the insulin response to intravenous glucose in obese insulin resistant high-fat fed C57BL/6J mice (P=0.041). After 60 min incubation of isolated islets from normal mice, insulin secretion in the presence of 16.7 mmol/l glucose was inhibited by apelin-36 at 1 pmol/l, whereas apelin-36 did not significantly affect insulin secretion at 2.8 or 8.3 mmol/l glucose or after stimulation of insulin secretion by KCI. Islet glucose oxidation at 16.7 mmol/l was not affected by apelin-36. We conclude that the apj receptor is expressed in pancreatic islets and that apelin-36 inhibits glucose-stimulated insulin secretion both in vivo and in vitro. This may suggest that the islet beta-cells are targets for apelin-36.},
  author       = {Sörhede Winzell, Maria and Magnusson, Caroline and Ahrén, Bo},
  issn         = {1873-1686},
  keyword      = {apj receptor,islets,mice,insulin secretion,apelin},
  language     = {eng},
  number       = {1-3},
  pages        = {12--17},
  publisher    = {Elsevier},
  series       = {Regulatory Peptides},
  title        = {The apj receptor is expressed in pancreatic islets and its ligand, apelin, inhibits insulin secretion in mice.},
  url          = {http://dx.doi.org/10.1016/j.regpep.2005.05.004},
  volume       = {131},
  year         = {2005},
}