Journal article
Whole body deletion of AMP-activated protein kinase β2 reduces muscle AMPK activity and exercise capacity
GR Steinberg, HM O'Neill, NL Dzamko, S Galic, T Naim, R Koopman, SB Jørgensen, J Honeyman, K Hewitt, ZP Chen, JD Schertzer, JW Scott, F Koentgen, GS Lynch, MJ Watt, BJW Van Denderen, DJ Campbell, BE Kemp
Journal of Biological Chemistry | ELSEVIER | Published : 2010
Open access
Abstract
AMP-activated protein kinase (AMPK) β subunits (β1 and β2) provide scaffolds for binding α and γ subunits and contain a carbohydrate-binding module important for regulating enzyme activity. We generated C57Bl/6 mice with germline deletion of AMPK β2 (β2 KO) and examined AMPK expression and activity, exercise capacity, metabolic control during muscle contractions, aminoimidazole carboxamide ribonucleotide (AICAR) sensitivity, and susceptibility to obesity-induced insulin resistance. We find that β2 KO mice are viable and breed normally. β2 KO mice had a reduction in skeletal muscle AMPK α1 and α2 expression despite up-regulation of the β1 isoform. Heart AMPK α2 expression was also reduced but..
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Awarded by Danish Medical Research Council
Funding Acknowledgements
This work was supported in part by grants from the Australian Research Council (to B. E. K.), National Health and Medical Research Council (to D. J. C., B. E. K., G. R. S., and M. J. W.), Natural Science and Engineering Research Council of Canada (to G. R. S.), Diabetes Australia Research Trust (to G. R. S.), and the National Heart Foundation of Australia (to B. E. K. and D. J. C.). Supported by a scholarship from the National Heart Foundation. Supported by Research Fellowship 271-05-0697 from the Danish Medical Research Council. Supported by research fellowships from the National Health and Medical Research Council of Australia.