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Einfluss von Vitamin D auf Knochen und Muskel

Influence of vitamin D on bones and muscle

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Zusammenfassung

Vitamin-D-Metabolismus

Vitamin D wird in der Leber in die Speicherform 25-Hydroxy-Vitamin D umgewandelt. Die weitere Aktivierung zum Hormon 1,25-Dihydroxy-Vitamin D (Kalzitriol) findet streng reguliert in der Niere statt, kann aber auch lokal in Zielorganen erfolgen, z. B. auch in Knochenzellen. Effekte auf Muskel und Knochen zählen zu den klassischen Vitamin-D-Wirkungen. Kalzitriol wirkt am Muskel über den nukleären Vitamin-D-Rezeptor, daneben aber auch über nichtgenomische Wege. Es steigert die Synthese von Muskelproteinen und moduliert die Differenzierung der Muskelzellen.

Vitamin-D-Mangel

Er führt zu Muskelschwäche (typisch für Rachitis und Osteomalazie). Interventionsstudien zeigten bei älteren Menschen mit Vitamin-D-Mangel eine Verbesserung der Muskelfunktion mit Reduktion der Sturzrate durch Vitamin-D-Gabe. Am Knochen hat Kalzitriol sowohl anabole als auch katabole Effekte. Infolge verbesserter intestinaler Absorption wird mehr Kalzium und Phosphat zur Mineralisierung zur Verfügung gestellt. Kalzitriol wirkt zudem direkt auf die Proliferation und Differenzierung von Knochenzellen und auf die Bildung von alkalischer Phosphatase und Matrixproteinen (z. B. Osteokalzin, Osteopontin). Somit reguliert es die Mineralisation im Knochen in direkter Weise. In hohen Konzentrationen stimuliert Kalzitriol aber auch die Knochenresorption. Personen mit ausgeprägtem Vitamin-D-Mangel weisen ein erhöhtes Knochenbruchrisiko auf. Dieses kann durch Vitamin-D-Supplementierung verringert werden.

Vitamin-D-Supplementierung

Als optimal wird die tägliche Dosierung mit 800–2000 IU Vitamin D3 angesehen. In der Pharmakotherapie metabolischer Osteopathien verbessern aktive Metaboliten (Kalzitriol, Alfakalzidol, Parikalzitol) Sturzhäufigkeit und Muskelfunktion und senken die Frakturrate.

Abstract

Vitamin D metabolism

Vitamin D is converted in the liver to 25-hydroxyvitamin D, which represents the storage form and is the most abundant circulating metabolite. The further activation (1-α-hydroxylation) leads to the hormone 1‑α,25-dihydroxyvitamin D (calcitriol), which takes place in the kidneys under hormonal control and contributes to circulating calcitriol but some target organs (such as bone) can produce calcitriol in an autocrine/paracrine fashion. Muscle and bone are the classical target organs for calcitriol. The hormone calcitriol has direct effects on muscle tissue, which are mediated by the nuclear vitamin D receptor (VDR) and also by non-genomic pathways (membrane receptors). Calcitriol modulates differentiation of muscle cells and stimulates protein synthesis.

Vitamin D deficiency

Vitamin D deficiency leads to muscle weakness, which is prominent in patients with rickets and osteomalacia; however, even subclinical vitamin D deficiency is associated with diminished muscle function. In populations with vitamin D deficiency (e. g. elderly people), controlled intervention studies with vitamin D demonstrated improved muscle function and reduction in falls. In bone, calcitriol exerts anabolic and catabolic effects. Calcitriol stimulates intestinal absorption of calcium and phosphate providing mineral supply for bone mineralization. Calcitriol also has direct effects on proliferation and differentiation of bone cells. Calcitriol stimulates alkaline phosphatase and regulates bone matrix proteins (such as osteocalcin and osteopontin); therefore, calcitriol regulates mineralization in a direct manner. In high concentrations calcitriol also stimulates bone resorption. People with severe vitamin D deficiency have a higher risk for fractures. Vitamin D supplementation can reduce the risk of fractures.

Vitamin D supplementation

The best evidence exists for the daily administration of 800–2000 IU of vitamin D. Active vitamin D metabolites (also called vitamin D receptor agonists), such as calcitriol, alfacalcidol (1-α-hydroxyvitamin D) and paricalcitol are used for the pharmacological treatment of metabolic bone diseases and in these conditions reduce falls, improve muscle function and reduce the risk of fractures.

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  1. Praxis Endokrinologie & Diabetologie, Salinenstraße 8, 83435, Bad Reichenhall, Deutschland

    S. Scharla

  2. Medizinische Fakultät, Ludwig-Maximilians-Universität München, München, Deutschland

    S. Scharla

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Scharla, S. Einfluss von Vitamin D auf Knochen und Muskel. Diabetologe 12, 261–268 (2016). https://doi.org/10.1007/s11428-016-0101-x

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