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Введение

Изначально было выявлено, что дефицит витамина D является причиной развития рахита, при недостаточном воздействии солнечного света или употреблении пищи, бедной витамином D. Это заболевание до сих пор является эндемичным в большинстве стран мира [1]. Впоследствии несколько мета-анализов показали, что прием витамина D и кальция снижает риск остеопоротических переломов у пожилых людей.

Помимо своей роли в регуляции кальциевого обмена и костного гомеостаза, витамин D участвует в регуляции многих других клеточных функций. Рецепторы витамина D (VDR - vitamin D receptor) экспрессируются почти во всех ядросодержащих клетках. Около 3% генома человека и мыши регулируется 1,25-дигидроксивитамином D - активной формой витамина D. Более того, по меньшей мере 10 тканей за пределами почек экспрессируют фермент 1-альфа-гидроксилазу (CYP27B1), который отвечает за преобразование витамина D в его активную форму. Таким образом, активный гормон может синтезироваться ауто- или паракринным путем. Это означает, что спектр эyдокринной активности витамина D значительно шире, чем просто регуляция кальциевого обмена и поддержание костного гомеостаза. В этом отношении система витамин D–VDR схожа с системой других лигандов ядерных рецепторов, таких как гормоны щитовидной железы [2-4].

Оптимальный уровень витамина D для здоровья внескелетных органов и систем

Мышечная функция

Онкологические заболевания

Иммунная система

Сердечно-сосудистая система

Диабет

Нейропсихиатрическая функция

Беременность и дети

Смертность

Гены и уровень витамина D

Резюме и рекомендации

Список литературы