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AMPK regulates contraction‐induced glucose uptake in situ but not ex vivo
Author(s) -
Fentz Joachim,
Pehmøller Christian,
Treebak Jonas Thue,
Kjoebsted Rasmus,
Viollet Benoit,
Wojtaszewski Jørgen
Publication year - 2013
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.27.1_supplement.1202.12
Subject(s) - ampk , ex vivo , skeletal muscle , in vivo , extensor digitorum longus muscle , chemistry , in situ , stimulation , contraction (grammar) , medicine , endocrinology , soleus muscle , protein kinase a , biology , phosphorylation , biochemistry , in vitro , microbiology and biotechnology , organic chemistry
The use of transgenic models studying the role of 5′AMP‐activated protein kinase (AMPK) in contraction‐induced glucose uptake (CTGU) has led to inconclusive results. Drawbacks of using less appropriate models displaying incomplete abrogation of AMPKα catalytic activity may explain these differences. The purpose of this study was to determine whether a total lack of both AMPK α1 and α2 catalytic subunits abolishes CTGU in muscle under ex vivo and in situ conditions. We generated a skeletal muscle specific AMPK‐α1 and‐α2 double knock‐out (dKO) mouse model. Electrical stimulation was applied directly to the muscle (ex vivo, 10 min (either 1 or 2 second trains/15 seconds)) or to the sciatic nerve (in situ, 15 min (1 train/second) +30 min recovery) to stimulate contraction. Muscle glucose uptake was measured using radioactively labeled isotopes. Ex vivo CTGU in AMPKα WT and dKO soleus and extensor digitorum longus (EDL) muscles was similar between genotypes. Equal force production was registered under all of the above conditions. Contrary to the ex vivo data, the CTGU in situ was impaired by ~50% in the tibialis anterior, soleus and EDL muscles of AMPKα dKO mice compared to WT mice (p<0.05). Basal non stimulated glucose uptake was similar between genotypes, both ex vivo and in situ. The results suggest that AMPK's role in CTGU may be modulated by a factor(s) related to muscle perfusion and/or stimulation methodology.