5`-aminoimidazole-4-carboxyamide-ribonucleoside- activated glucose transport is not prevented by nitric oxide synthase inhibition in rat isolated skeletal muscle

Stephens, T, Canny, B, Snow, Rod and McConell, G 2004, 5`-aminoimidazole-4-carboxyamide-ribonucleoside- activated glucose transport is not prevented by nitric oxide synthase inhibition in rat isolated skeletal muscle, Clinical and experimental pharmacology and physiology, vol. 31, no. 7, pp. 419-423.

Attached Files
Name Description MIMEType Size Downloads

Title 5`-aminoimidazole-4-carboxyamide-ribonucleoside- activated glucose transport is not prevented by nitric oxide synthase inhibition in rat isolated skeletal muscle
Author(s) Stephens, T
Canny, B
Snow, Rod
McConell, G
Journal name Clinical and experimental pharmacology and physiology
Volume number 31
Issue number 7
Start page 419
End page 423
Publisher Blackwell Scientific Publications
Place of publication Oxford, England
Publication date 2004
ISSN 0305-1870
Keyword(s) AMP-activated protein kinase
contraction
exercise
glucose transport
nitric oxide synthase inhibition
nitric oxide synthase
skeletal muscle
Summary 1. The nucleoside intermediate 5'-aminoimidazole-4-carboxyamide-ribonucleoside (AICAR) activates skeletal muscle AMP-activated protein kinase (AMPK) and increases glucose uptake. The AMPK phosphorylates neuronal nitric oxide synthase (nNOS)µ in skeletal muscle fibres. There is evidence that both AMPK and nNOSµ may be involved in the regulation of contraction-stimulated glucose uptake.
2. We examined whether both AICAR- and contraction-stimulated glucose uptake were mediated by NOS in rat skeletal muscle.
3. Rat isolated epitrochlearis muscles were subjected in vitro to electrically stimulated contractions for 10 min and/or incubated in the presence or absence of AICAR (2 mmol/L) or the NOS inhibitor NG-monomethyl-l-arginine (l-NMMA; 100 µmol/L).
4. Muscle contraction significantly (P < 0.05) altered the metabolic profile of the muscle. In contrast, AICAR and l-NMMA had no effect on the metabolic profile of the muscle, except that AICAR increased muscle 5'-aminoimidazole-4-carboxyamide-ribonucleotide (ZMP) and AICAR content. Nitric oxide synthase inhibition caused a small but significant (P < 0.05) reduction in basal 3-O-methylglucose transport, which was observed in all treatments. 5'-Aminoimidazole-4-carboxyamide-ribonucleoside significantly increased (P < 0.05) glucose transport above basal, with NOS inhibition decreasing this slightly (increased by 209% above basal compared with 184% above basal with NOS inhibition). Contraction significantly increased glucose transport above basal, with NOS inhibition substantially reducing this (107% increase vs 31% increase). 5'-Aminoimidazole-4-carboxyamide-ribonucleoside plus contraction in combination were not additive on glucose transport.
5. These results suggest that NO plays a role in basal glucose uptake and may regulate contraction-stimulated glucose uptake. However, NOS/nitric oxide do not appear to be signalling intermediates in AICAR-stimulated skeletal muscle glucose uptake.
Language eng
Field of Research 060602 Animal Physiology - Cell
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2008, Blackwell Publishing Asia Pty Ltd
Persistent URL http://hdl.handle.net/10536/DRO/DU:30008701

Connect to link resolver
 
Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved.

Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 19 times in TR Web of Science
Scopus Citation Count Cited 21 times in Scopus
Google Scholar Search Google Scholar
Access Statistics: 429 Abstract Views, 0 File Downloads  -  Detailed Statistics
Created: Mon, 13 Oct 2008, 15:39:31 EST

Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.