Effects of chronic dietary creatine feeding on cardiac energy metabolism and on creatine content in heart, skeletal muscle, brain, liver and kidney

被引:46
作者
Horn, M
Frantz, S
Remkes, H
Laser, A
Urban, B
Mettenleiter, A
Schnackerz, K
Neubauer, S
机构
[1] Univ Wurzburg, Med Klin, D-97080 Wurzburg, Germany
[2] Univ Wurzburg, Theodor Boveri Inst Biowissensch, D-97080 Wurzburg, Germany
关键词
creatine metabolism; cardiac energy reserve; P-31-NMR spectroscopy; isolated rat heart; ATP; phosphocreatine;
D O I
10.1006/jmcc.1997.0590
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Little is known about the regulation of total creatine concentration in heart, skeletal muscle, brain, liver and kidney in response to increased dietary creatine intake. The phosphorylated fraction of intracellular creatine (phosphocreatine) remain relatively constant, and therefore, higher intracellular creatine levels may increase the energy reserve of the heart [phosphocreatine and phosphoryl transfer via creatine kinase (CK)] and of other organs. To test the effect of supplying exogenous creatine on the myocardial energy reserve and on creatine content of various organs, rats were given chow containing 0 (Untreated), 1, 3, 5, or 7% (of diet weight) creatine for similar to 40 days. Thereafter, hearts were perfused and left Ventricular developed pressure and heart rate were recorded. High energy phosphate concentrations were determined with P-31-NMR spectroscopy, CK reaction velocity by P-31-magnetization transfer. Total creatine was determined in heart, skeletal muscle, brain, liver, kidney and serum by high-performance liquid chromatography (HPLC), Creatine feeding increased serum creatine by 73% (1% creatine), 142% (3%), 166% (5%) and 202% (7%). In the heart, increased serum creatine levels did not affect mechanical function; ATP, phosphocreatine, inorganic phosphate, CK reaction velocity and total creatine were all unchanged. Total creatine also remained constant in brain and skeletal muscle, while creatine content increased 4.6-fold in the liver and 1.9-fold in the kidney. We conclude that myocardial energy reserve via CK cannot be increased by exogenous creatine treatment. (C) 1998 Academic Press Limited.
引用
收藏
页码:277 / 284
页数:8
相关论文
共 25 条
[1]   STUDY OF MODERATELY RAPID CHEMICAL EXCHANGE REACTIONS BY MEANS OF NUCLEAR MAGNETIC DOUBLE RESONANCE [J].
FORSEN, S ;
HOFFMAN, RA .
JOURNAL OF CHEMICAL PHYSICS, 1963, 39 (11) :2892-&
[2]  
GUIMBAL C, 1993, J BIOL CHEM, V268, P8418
[3]   ELEVATION OF CREATINE IN RESTING AND EXERCISED MUSCLE OF NORMAL SUBJECTS BY CREATINE SUPPLEMENTATION [J].
HARRIS, RC ;
SODERLUND, K ;
HULTMAN, E .
CLINICAL SCIENCE, 1992, 83 (03) :367-374
[4]   Preservation of left ventricular mechanical function and energy metabolism in rats after myocardial infarction by the angiotensin-converting enzyme inhibitor quinapril [J].
Horn, M ;
Neubauer, S ;
Frantz, S ;
Hugel, S ;
Hu, K ;
Gaudron, P ;
Schnackerz, K ;
Ertl, G .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 1996, 27 (02) :201-210
[5]   Protective effect of the specific endothelin-1 antagonist BQ610 on mechanical function and energy metabolism during ischemia reperfusion injury in isolated perfused rat hearts [J].
Illing, B ;
Horn, M ;
Han, H ;
Hahn, S ;
Bureik, P ;
Ertl, G ;
Neubauer, S .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 1996, 27 (04) :487-494
[6]  
INGWALL JS, 1993, CIRCULATION, V87, P58
[7]  
LAWSON JWR, 1979, J BIOL CHEM, V254, P6528
[8]  
LEHNINGER AL, 1982, PRINCIPLES BIOCH, P467
[9]   EXTRACELLULAR CREATINE REGULATES CREATINE TRANSPORT IN RAT AND HUMAN-MUSCLE CELLS [J].
LOIKE, JD ;
ZALUTSKY, DL ;
KABACK, E ;
MIRANDA, AF ;
SILVERSTEIN, SC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (03) :807-811
[10]  
LOWRY OH, 1951, J BIOL CHEM, V193, P265