Premium
Mechanical signal transduction in glucose transport of murine extensor digitorum longus (EDL) muscle
Author(s) -
Smith Melissa Anne,
Moylan Jennifer S,
Reid Michael B
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1355-d
Subject(s) - ampk , catalase , chemistry , glucose transporter , phosphorylation , superoxide dismutase , reactive oxygen species , stimulation , skeletal muscle , medicine , signal transduction , biochemistry , endocrinology , microbiology and biotechnology , enzyme , protein kinase a , biology , insulin
Contraction in skeletal muscle leads to increased endogenous ROS production, AMPK activation and increased glucose transport. Our current study tested the hypothesis that mechanical stimulation, i.e. stretch, is sufficient to increase AMPK phosphorylation and glucose transport and that these increases are ROS sensitive. We previously have shown that stretching EDL increases oxidant activity (+150%, p<0.01), as measured by 2′,7′ dichlorofluorescein. This activity is suppressed by the ROS‐specific antioxidants superoxide dismutase (SOD) and catalase (p<0.05). We show that stretching EDL increases AMPK phosphorylation (+164% control, p<0.05) as measured by immunoblotting with a phospho‐specific antibody (Cell Signaling). This phosphorylation is suppressed by SOD and catalase (p<0.05). Finally, stretch increased glucose transport (+250% control, p<0.01), as measured by uptake of deoxy‐D[1,2‐ 3 H]glucose. In contrast to AMPK activity, stretch‐stimulated glucose transport was unaffected by SOD and catalase. These data demonstrate that while stretch‐stimulated AMPK activity is ROS sensitive, stretch‐stimulated glucose transport thus far appears to be ROS insensitive. Under these conditions, these data suggest that stretch‐stimulated glucose transport may not be AMPK mediated. Supported by AHA 0615263B & DK 066232.