Papers

Peer-reviewed
Jan, 2009

Uniaxial Cyclic Stretch Increases Glucose Uptake into C2C12 Myotubes through a Signaling Pathway Independent of Insulin-like Growth Factor I

HORMONE AND METABOLIC RESEARCH
  • M. Iwata
  • ,
  • S. Suzuki
  • ,
  • K. Hayakawa
  • ,
  • T. Inoue
  • ,
  • K. Naruse

Volume
41
Number
1
First page
16
Last page
22
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.1055/s-0028-1087170
Publisher
GEORG THIEME VERLAG KG

Insulin-like growth factor I (IGF-I), an autocrine/paracrine growth factor involved in myogenesis, has rapid effects on muscle metabolism. In a manner analogous to insulin and mechanical stimuli such as stretch, IGIF-I stimulates glucose transport through recruitment of glucose transporters to surface membranes in skeletal muscles. It is known that IGF-I is secreted from skeletal muscle cells in response to stretch. Therefore, we examined whether IGF-I is involved in the mechanism by which mechanical stretch regulates glucose transport using cultured C2C12 myotubes. IGF-I increased 2-deoxy-D-glucose (2-DG) uptake, and this created an additive effect with mechanical stretch, suggesting that these stimuli enhance glucose transport through different mechanisms. In fact, IGF-I-stimulated 2-DG uptake was not blocked by dantrolene (an inhibitor of Ca2+ release from sarcoplasmic reticulum), whereas the stretch-stimulated effect was abolished. Conversely, the IGF-I-stimulated 2-DG uptake was prevented by phosphatidylinositol 3-kinase inhibitor wortmannin, which did not prevent the stretch-stimulated 2-DG uptake. In addition, experiments using media conditioned by stretched myotubes indicated that a mechanically induced release of locally acting autocrine/paracrine growth factors was not sufficient for induction of 2-DG uptake. Thus, our results demonstrate that mechanical stretch signaling for glucose transport is independent of the mechanism through which IGF-I increases this transport.

Link information
DOI
https://doi.org/10.1055/s-0028-1087170
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000262778200004&DestApp=WOS_CPL
ID information
  • DOI : 10.1055/s-0028-1087170
  • ISSN : 0018-5043
  • eISSN : 1439-4286
  • Web of Science ID : WOS:000262778200004

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