Dietary NaCl supplementation prevents muscle necrosis in a mouse model of Duchenne muscular dystrophy

1 Department of Degenerative Neurological Disease, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan; 2 Hitachi High Technologies, Ibaraki, Japan Submitted 5 October 2004 ; accepted in final form 13 September 2005 The mdx mouse is an animal model for Duche...

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Published in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2006-02, Vol.290 (2), p.R449-R455
Main Authors: Yoshida, Mizuko, Yonetani, Akira, Shirasaki, Toshihiro, Wada, Keiji
Format: Article
Language:English
Subjects:
Aging
Animals
Calcium - blood
Calcium - metabolism
Creatine Kinase - metabolism
Dietary Supplements
Disease Models, Animal
Drug Administration Routes
Female
Male
Mice
Mice, Inbred mdx
Muscle, Skeletal - drug effects
Muscle, Skeletal - pathology
Muscular Dystrophy, Duchenne - diet therapy
Muscular Dystrophy, Duchenne - pathology
Necrosis - prevention & control
Potassium - blood
Potassium - metabolism
Sodium - blood
Sodium - metabolism
Sodium Chloride - administration & dosage
Sodium Chloride - pharmacology
Zinc - metabolism
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Summary:1 Department of Degenerative Neurological Disease, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan; 2 Hitachi High Technologies, Ibaraki, Japan Submitted 5 October 2004 ; accepted in final form 13 September 2005 The mdx mouse is an animal model for Duchenne muscular dystrophy. Mdx mice fed a 12% NaCl diet from birth up to 20 days of age (mdx-Na mice) had an 50% reduction in serum creatine kinase (CK) activity compared with mdx mice fed a standard diet. Most notably, necrotic fibers in tibialis anterior (TA) muscle of mdx-Na mice were reduced by 99% and were similar in control mice. These mdx mice displayed significantly elevated blood Ca 2+ and Na + levels, while the total calcium content of their TA muscle was reduced to the level of control mice. In addition, mdx-Na mice had elevated zinc and magnesium contents in their TA muscle. These results suggest that elevated serum Na + leads to Ca 2+ extrusion from muscle via the Na + /Ca 2+ exchanger causing a decrease in intracellular Ca 2+ levels and an increase in blood Ca 2+ levels. Extracellular Ca 2+ and, in addition, Zn 2+ and Mg 2+ might also contribute to the stabilization of the cell membrane. Other possibilities explaining the surprisingly efficacious beneficial effect of dietary sodium exist and are discussed. therapy; calcium and zinc; potassium; blood; serum creatine kinase activity Address for reprint requests and other correspondence: Mizuko Yoshida, Department of Degenerative Neurological Disease, National Institute of Neuroscience, NCNP, 4-1-1 Ogawahigashi, Kodaira, Tokyo 187–8052, Japan (e-mail: yoshidam{at}ncnp.go.jp )
ISSN:0363-6119
1522-1490
DOI:10.1152/ajpregu.00684.2004