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低磷血症是导致维生素 D 缺乏性骨骼肌无力的原因。

Hypophosphatemia is responsible for skeletal muscle weakness of vitamin D deficiency.

机构信息

Department of Biochemistry, University of Wisconsin-Madison, 53706-1544, United States.

出版信息

Arch Biochem Biophys. 2010 Aug 15;500(2):157-61. doi: 10.1016/j.abb.2010.05.029. Epub 2010 May 31.

Abstract

A deficiency of vitamin D results in muscle weakness as well as rickets in children and osteomalacia in the adult. To study the basis for this weakness, severe vitamin D deficiency was produced in rats as revealed by a low level or absence of 25-hydroxyvitamin D(3) in the serum. Vitamin D deficiency was achieved by feeding purified diets to weanlings for 16 weeks. Muscle force, peak contraction (P), time-to-half contraction (T(1/2)), time-to-peak contraction (T(P)), and time-to-half recovery (T(1/2r)) were measured. A significant reduction in muscle force was found when vitamin D deficiency was accompanied by hypophosphatemia. Within 2 days of correcting the hypophosphatemia, muscle strength was normalized. When serum calcium and serum phosphorus were maintained in the normal range in vitamin D-deficient rats, muscle weakness did not develop. Further, hypocalcemia together with vitamin D deficiency did not produce muscle weakness. These results strongly suggest that muscle weakness noted in rachitic patients is the result of the hypophosphatemia of vitamin D deficiency.

摘要

维生素 D 缺乏会导致肌肉无力,儿童出现佝偻病,成人出现骨软化症。为了研究这种虚弱的基础,通过在血清中检测到低水平或缺乏 25-羟维生素 D(3),在大鼠中产生严重的维生素 D 缺乏。通过用纯化饮食喂养断奶大鼠 16 周来实现维生素 D 缺乏。测量肌肉力量、峰值收缩(P)、半收缩时间(T(1/2))、收缩至峰值时间(T(P))和半恢复时间(T(1/2r))。当维生素 D 缺乏伴有低磷血症时,发现肌肉力量显著降低。在纠正低磷血症后 2 天内,肌肉力量恢复正常。当维生素 D 缺乏的大鼠的血清钙和血清磷保持在正常范围内时,不会出现肌肉无力。此外,低钙血症与维生素 D 缺乏一起不会导致肌肉无力。这些结果强烈表明,佝偻病患者出现的肌肉无力是维生素 D 缺乏导致低磷血症的结果。

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