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J Physiol Sci. 2019 Jul;69(4):661-671. doi: 10.1007/s12576-019-00683-8. Epub 2019 May 11.

Renal involvement in the pathogenesis of mineral and bone disorder in dystrophin-deficient mdx mouse.

Author information

1
Department of Pathophysiology, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku, Tokyo, 160-8402, Japan. ewada@tokyo-med.ac.jp.
2
Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro, Tokyo, 153-8902, Japan. ewada@tokyo-med.ac.jp.
3
Department of Comprehensive Kidney Disease Research, Osaka University Graduate of School Medicine, B6-2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
4
Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro, Tokyo, 153-8902, Japan.
5
Department of Pathophysiology, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku, Tokyo, 160-8402, Japan.
6
Graduate School of Science, Tokyo University of Science, 1-3 Kagurazaka, Shinjuku, Tokyo, 162-8601, Japan.

Abstract

Duchenne muscular dystrophy is a severe muscular disorder, often complicated with osteoporosis, and impaired renal function has recently been featured. We aimed to clarify the involvement of renal function in the pathogenesis of mineral and bone disorder in mdx mice, a murine model of the disease. We clearly revealed renal dysfunction in adult mdx mice, in which dehydration and hypercalcemia were contributed. We also examined the effects of dietary phosphorus (P) overload on phosphate metabolism. Serum phosphate and parathyroid hormone (PTH) levels were significantly increased in mdx mice by dietary P in a dose-dependent manner; however, bone alkaline phosphatase levels were significantly lower in mdx mice. Additionally, bone mineral density in mdx mice were even worsened by increased dietary P in a dose-dependent manner. These results suggested that the uncoupling of bone formation and resorption was enhanced by skeletal resistance to PTH due to renal failure in mdx mice.

KEYWORDS:

Duchenne muscular dystrophy; Mineral and bone disorder; Osteoporosis; Phosphate overloading; Renal dysfunction

PMID:
31079351
DOI:
10.1007/s12576-019-00683-8

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