A(1) receptor deficiency causes increased insulin and glucagon secretion in mice
Johansson, Stina M. ; Salehi, S Albert LU
; Sandstroem, Marie E.
; Westerblad, Hakan
; Lundquist, Ingmar
LU
; Carlsson, Per-Ola
; Fredholm, Bertil B.
and Katz, Abram
(2007)
In Biochemical Pharmacology
74(11).
p.1628-1635
- Abstract
- Adenosine influences metabolism and the adenosine receptor antagonist caffeine decreases the risk of type 2 diabetes. In this study the metabolic role of one adenosine receptor subtype, the adenosine A(1)R, was evaluated in mice lacking this receptor [A(1)R (-/-)]. The HbA1c levels and body weight were not significantly different between wild type [A(1)R (+/+)] and A(1)R (-/-) mice (3-4 months) fed normal lab chow. At rest, plasma levels of glucose, insulin and glucagon were similar in both genotypes. Following glucose injection, glucose tolerance was not appreciably altered in A(1)R (-/-) mice. Glucose injection induced sustained increases in plasma insulin and glucagon levels in A(1)R (-/-) mice, whereas A(1)R (+/+) control mice reacted... (More)
- Adenosine influences metabolism and the adenosine receptor antagonist caffeine decreases the risk of type 2 diabetes. In this study the metabolic role of one adenosine receptor subtype, the adenosine A(1)R, was evaluated in mice lacking this receptor [A(1)R (-/-)]. The HbA1c levels and body weight were not significantly different between wild type [A(1)R (+/+)] and A(1)R (-/-) mice (3-4 months) fed normal lab chow. At rest, plasma levels of glucose, insulin and glucagon were similar in both genotypes. Following glucose injection, glucose tolerance was not appreciably altered in A(1)R (-/-) mice. Glucose injection induced sustained increases in plasma insulin and glucagon levels in A(1)R (-/-) mice, whereas A(1)R (+/+) control mice reacted with the expected transient increase in insulin and decrease in glucagon levels. Pancreas perfusion experiments showed that A(1)R (-/-) mice had a slightly higherbasal insulin secretion than A(1)R (+/+) mice. The first phase insulin secretion (initiated with 16.7 mM glucose) was of the same magnitude in both genotypes, but the second phase was significantly enhanced in the A(1)R (-/-) pancreata compared with A(1)R (+/+). Insulin- and contraction-mediated glucose uptake in skeletal muscle were not significantly different between in A(1)R (-/-) and A(1)R (+/+) mice. All adenosine receptors were expressed at mRNA level in skeletal muscle in A(1)R (+/+) mice and the mRNA A(2A)R, A(2B)R and A(3)R levels were similar in A(1)R (-/-) and A(1)R (+/+) mice. In conclusion, the A(1)R minimally affects muscle glucose uptake, but is important in regulating pancreatic islet function. (c) 2007 Elsevier Inc. All rights reserved. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/969310
- author
- Johansson, Stina M.
; Salehi, S Albert
LU
; Sandstroem, Marie E.
; Westerblad, Hakan
; Lundquist, Ingmar
LU
; Carlsson, Per-Ola
; Fredholm, Bertil B.
and Katz, Abram
- organization
- publishing date
- 2007
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- A(1) receptor, glucose uptake, insulin sensitivity, islet hormone secretion, adenosine, metabolism
- in
- Biochemical Pharmacology
- volume
- 74
- issue
- 11
- pages
- 1628 - 1635
- publisher
- Elsevier
- external identifiers
-
- wos:000251118600008
- scopus:35349004692
- ISSN
- 0006-2952
- DOI
- 10.1016/j.bcp.2007.08.006
- language
- English
- LU publication?
- yes
- id
- 2f418577-a0f6-4369-b3ae-11aa319fb791 (old id 969310)
- date added to LUP
- 2016-04-01 11:47:13
- date last changed
- 2022-01-26 18:13:29
@article{2f418577-a0f6-4369-b3ae-11aa319fb791,
abstract = {{Adenosine influences metabolism and the adenosine receptor antagonist caffeine decreases the risk of type 2 diabetes. In this study the metabolic role of one adenosine receptor subtype, the adenosine A(1)R, was evaluated in mice lacking this receptor [A(1)R (-/-)]. The HbA1c levels and body weight were not significantly different between wild type [A(1)R (+/+)] and A(1)R (-/-) mice (3-4 months) fed normal lab chow. At rest, plasma levels of glucose, insulin and glucagon were similar in both genotypes. Following glucose injection, glucose tolerance was not appreciably altered in A(1)R (-/-) mice. Glucose injection induced sustained increases in plasma insulin and glucagon levels in A(1)R (-/-) mice, whereas A(1)R (+/+) control mice reacted with the expected transient increase in insulin and decrease in glucagon levels. Pancreas perfusion experiments showed that A(1)R (-/-) mice had a slightly higherbasal insulin secretion than A(1)R (+/+) mice. The first phase insulin secretion (initiated with 16.7 mM glucose) was of the same magnitude in both genotypes, but the second phase was significantly enhanced in the A(1)R (-/-) pancreata compared with A(1)R (+/+). Insulin- and contraction-mediated glucose uptake in skeletal muscle were not significantly different between in A(1)R (-/-) and A(1)R (+/+) mice. All adenosine receptors were expressed at mRNA level in skeletal muscle in A(1)R (+/+) mice and the mRNA A(2A)R, A(2B)R and A(3)R levels were similar in A(1)R (-/-) and A(1)R (+/+) mice. In conclusion, the A(1)R minimally affects muscle glucose uptake, but is important in regulating pancreatic islet function. (c) 2007 Elsevier Inc. All rights reserved.}},
author = {{Johansson, Stina M. and Salehi, S Albert and Sandstroem, Marie E. and Westerblad, Hakan and Lundquist, Ingmar and Carlsson, Per-Ola and Fredholm, Bertil B. and Katz, Abram}},
issn = {{0006-2952}},
keywords = {{A(1) receptor; glucose uptake; insulin sensitivity; islet hormone secretion; adenosine; metabolism}},
language = {{eng}},
number = {{11}},
pages = {{1628--1635}},
publisher = {{Elsevier}},
series = {{Biochemical Pharmacology}},
title = {{A(1) receptor deficiency causes increased insulin and glucagon secretion in mice}},
url = {{http://dx.doi.org/10.1016/j.bcp.2007.08.006}},
doi = {{10.1016/j.bcp.2007.08.006}},
volume = {{74}},
year = {{2007}},
}