PMID- 10516614
OWN - NLM
STAT- MEDLINE
DCOM- 19991222
LR  - 20191103
IS  - 0952-3480 (Print)
IS  - 0952-3480 (Linking)
VI  - 12
IP  - 6
DP  - 1999 Oct
TI  - Effects of ischemia on skeletal muscle energy metabolism in mice lacking creatine
      kinase monitored by in vivo 31P nuclear magnetic resonance spectroscopy.
PG  - 327-34
AB  - The aim of this study was to provide in vivo experimental evidence for the
      proposed biological significance of the creatine kinase (CK)/phosphocreatine
      (PCr) system in the energy metabolism of skeletal muscle. As a test system we
      compared hindlimb muscle of knockout mice lacking the cytosolic M-type
      (M-CK(-)/(-)), the mitochondrial ScMit-type (ScCKmit(-)/(-)), or both creatine
      kinase isoenzymes (CK(-)/(-)), and in vivo 31P-NMR was used to monitor metabolic 
      responses during and after an ischemic period. Although single mutants show some 
      subtle specific abnormalities, in general their metabolic responses appear
      similar to wild type, in contrast to CK(-)/(-) double mutants. This implies that 
      presence of one CK isoform is both necessary and sufficient for the system to be 
      functional in meeting ischemic stress conditions. The global ATP buffering role
      of the CK/PCr system became apparent in a 30% decline of ATP in the CK(-)/(-)
      mice during ischemia. Both M-CK(-)/(-) and CK(-)/(-) showed increased
      phosphomonoester levels during ischemia, most likely reflecting adaptation to a
      more efficient utilization of glycogenolysis. While in M-CK(-)/(-) muscle PCr can
      still be hydrolyzed to provide Pi for this process, in CK(-)/(-) muscle only Pi
      from ATP breakdown is available and Pi levels increase much more slowly. The
      experiments also revealed that the system plays a role in maintaining pH levels; 
      the CK(-)/(-) mice showed a faster and more pronounced acidification (pH = 6.6)
      than muscles of wild type and single knockout mutants (pH = 6.9).
CI  - Copyright 1999 John Wiley & Sons, Ltd.
FAU - in 't Zandt, H J
AU  - in 't Zandt HJ
AD  - Department of Radiology, University Hospital Nijmegen, 6500 HB, Nijmegen, The
      Netherlands. R.intZandt@rdiag.azn.nl
FAU - Oerlemans, F
AU  - Oerlemans F
FAU - Wieringa, B
AU  - Wieringa B
FAU - Heerschap, A
AU  - Heerschap A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - NMR Biomed
JT  - NMR in biomedicine
JID - 8915233
RN  - 0 (Isoenzymes)
RN  - 0 (Lactates)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - 9005-79-2 (Glycogen)
RN  - EC 2.7.3.2 (Creatine Kinase)
SB  - IM
MH  - Adenosine Triphosphate/metabolism
MH  - Animals
MH  - Creatine Kinase/*deficiency/*genetics/metabolism
MH  - Energy Metabolism/genetics
MH  - Female
MH  - Glycogen/metabolism
MH  - Glycolysis
MH  - Ischemia/enzymology/genetics/*metabolism
MH  - Isoenzymes
MH  - Lactates/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Muscle, Skeletal/*blood supply/enzymology/*metabolism
MH  - Nuclear Magnetic Resonance, Biomolecular/methods
MH  - Oxidative Phosphorylation
EDAT- 1999/10/12 00:00
MHDA- 1999/10/12 00:01
CRDT- 1999/10/12 00:00
PHST- 1999/10/12 00:00 [pubmed]
PHST- 1999/10/12 00:01 [medline]
PHST- 1999/10/12 00:00 [entrez]
AID - 10.1002/(SICI)1099-1492(199910)12:6<327::AID-NBM570>3.0.CO;2-9 [pii]
AID - 10.1002/(sici)1099-1492(199910)12:6<327::aid-nbm570>3.0.co;2-9 [doi]
PST - ppublish
SO  - NMR Biomed. 1999 Oct;12(6):327-34. doi:
      10.1002/(sici)1099-1492(199910)12:6<327::aid-nbm570>3.0.co;2-9.