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Iron deficiency causes a shift in AMP‐activated protein kinase (AMPK) catalytic subunit composition in rat skeletal muscle
Author(s) -
Merrill John Floyd,
Hepworth Squire D.,
Willie Shelby,
Winder William W.,
Thomson David M.,
Hancock Chad R.
Publication year - 2012
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.26.1_supplement.1144.12
Subject(s) - ampk , medicine , endocrinology , amp activated protein kinase , protein subunit , skeletal muscle , protein kinase a , chemistry , stimulation , phosphocreatine , phosphorylation , acetyl coa carboxylase , biochemistry , enzyme , biology , pyruvate carboxylase , energy metabolism , gene
To determine effects of iron deficiency on LKB1/AMPK signaling, rats were fed a control (C=0.29 mg/g Fe) or iron deficient (ID=0 mg/g Fe) diet for 8 wks resulting in hematocrits of 47.5% ± 1.0% and 16.5% ± 0.6% respectively. Iron deficiency resulted in 28.3% greater muscle fatigue (p<0.01) in response to 10 min of stimulation (1 twitch/sec) and was associated with a greater reduction in phosphocreatine (C: 45.6%; ID: 85.9%) and ATP levels (C: 0%; ID: 24.0%). AMPK activation increased with stimulation in muscles of C and ID animals. A reduction in Cytochrome c and other heme‐containing mitochondrial proteins was observed in ID animals (p<0.01). The two isoforms of the AMPK catalytic subunit (α) are known to sense and respond differently to energy challenges. In ID animals, the AMPKα2 subunit protein content was reduced by 28.4% (p<0.05), however this did not result in a significant difference in resting AMPKα2 activity. AMPKα1 protein was unchanged, however an overall increase in AMPKα1 activity was observed (C: 1375.8 pmol/mg/min; ID: 2229.8 pmol/mg/min, p<0.01). Resting phospho Acetyl CoA Carboxylase (pACC) was also increased by 17‐fold (p<0.05), indicating greater AMPK activity that was not determined by the AMPK activity assay. This study indicates that chronic iron deficiency causes a shift in the expression of AMPKα subunit composition and potentially altered sensitivity to cellular energy challenges.