First Author | Yoshida M | Year | 2006 |
Journal | Am J Physiol Regul Integr Comp Physiol | Volume | 290 |
Issue | 2 | Pages | R449-55 |
PubMed ID | 16179484 | Mgi Jnum | J:115746 |
Mgi Id | MGI:3692146 | Doi | 10.1152/ajpregu.00684.2004 |
Citation | Yoshida M, et al. (2006) Dietary NaCl supplementation prevents muscle necrosis in a mouse model of Duchenne muscular dystrophy. Am J Physiol Regul Integr Comp Physiol 290(2):R449-55 |
abstractText | 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 approximately 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 Ca2+ 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 Ca2+ extrusion from muscle via the Na+/Ca2+ exchanger causing a decrease in intracellular Ca2+ levels and an increase in blood Ca2+ levels. Extracellular Ca2+ and, in addition, Zn2+ and Mg2+ 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. |