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Cross‐talk between CaMKII and AMPK is associated with increased FA metabolism in contracting rodent muscle
Author(s) -
Raney Marcella A.,
Turcotte Lorraine P.
Publication year - 2006
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.20.5.a1449-c
Subject(s) - ampk , caffeine , chemistry , endocrinology , medicine , stimulation , protein kinase a , contraction (grammar) , metabolism , muscle contraction , amp activated protein kinase , kinase , biochemistry , biology
Calcium‐calmodulin/dependent protein kinase II (CaMKII) and AMP‐activated protein kinase (AMPK) have individually been implicated in the regulation of muscle substrate metabolism during exercise. The purpose of this study was to determine whether CaMKII is involved in the regulation of FA metabolism and if it is involved, whether it does so independently of AMPK. Rat hindquarters were perfused at rest with (n=16) or without (n=15) 3mM caffeine or during electrical stimulation of moderate intensity (n=15). For each condition, rats were perfused in the presence of either 10μM KN92 or KN93, inactive and active CaMKII inhibitors respectively. For matched FA delivery, FA uptake and oxidation increased by 64% and 31% during caffeine treatment and 124% and 60% during electrical stimulation. KN93 had no effect on FA kinetics at rest ( P >0.05). However, KN93 completely abolished caffeine‐induced FA uptake, decreased contraction‐induced FA uptake by 32%, and completely abolished both caffeine‐ and contraction‐induced FA oxidation ( P <0.05). Caffeine and electrical stimulation resulted in a 67% and 3‐fold increase in AMPKα 2 activity respectively ( P <0.05). KN93 had no effect on caffeine‐induced AMPKα 2 activity ( P >0.05). Alternatively, it decreased contraction‐induced AMPKα 2 activity by 51% ( P <0.05) suggesting that cross‐talk is present between CaMKII and AMPK during muscle contraction. These results demonstrate that caffeine acts via CaMKII to increase FA metabolism and that regulation of contraction‐induced FA metabolism occurs in part via CaMKII possibly due to cross‐talk with AMPK. Supported by NIH AR‐45168 and USC WiSE program.