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AMPKα2 is not necessary to increase the activation state of ERK1/2, CaMKI, or AS160 during moderate intensity muscle contraction in perfused mouse muscle
Author(s) -
Abbott Marcia J,
Turcotte Lorraine P.
Publication year - 2010
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.24.1_supplement.1046.15
Subject(s) - ampk , chemistry , contraction (grammar) , skeletal muscle , medicine , endocrinology , phosphorylation , microbiology and biotechnology , biochemistry , biology , protein kinase a
AMPK has been implicated in the regulation of multiple metabolic signaling pathways and has been deemed an energy sensor during muscle contraction. The purpose of this study was to determine if AMPKα2 is required to measure alterations in the activation state of signaling molecules during caffeine treatment (C) and moderate intensity muscle contraction (MIMC). Male C57BL/6 mice were either wild type (WT) or skeletal and heart muscle specific dominant negative (DN) AMPKα2. Hindquarters were perfused with 550μM palmitate and 6mM glucose at rest (R; WT n=5 and DN n=6), during C (3mM; WT n=5 and DN n=5) and during MIMC (WT n=6 and DN n=5). Hindlimb muscles were freeze‐clamped in situ and used for analysis of protein expression and phosphorylation state. ACC~p increased ( P <0.05) 32 and 64% with C and MC. In the DN mice, ACC~pwas 11, 24, and 35% lower ( P <0.05) in the R, C, and MIMC groups when compared to similarly‐treated WT groups. ERK1/2~p increased ( P <0.05) 38% with MIMC. CaMKI~p increased ( P <0.05) 150 and 103% with C and MIMC. AS160~p increased ( P <0.05) 18 and 43% with C and MIMC. No genome‐induced differences were detected. Our results provide evidence for C‐ and MIMC‐induced activation of ACC, ERK1/2, CaMKI, and AS160 in a physiologically relevant muscle model and further suggest that AMPKα2 is not necessary to activate ERK1/2, CaMKI, or AS160 during C and MIMC in perfused mouse hindlimb muscle.