ESTUDIOS CIENTÍFICOS

Effects on Skeletal

Vitamin D—Effects on Skeletal and Extraskeletal Health and the Need for Supplementation

Matthias Wacker and Michael F. Holick *
Vitamin D, Skin and Bone Research Laboratory, Section of Endocrinology, Nutrition, and Diabetes, Department of Medicine, Boston University Medical Center, 85 East Newton Street, M-1013, Boston,
MA 02118, USA; E-Mail: mwacker@bu.edu
Received: 15 October 2012; in revised form: 21 November 2012 / Accepted: 13 December 2012 / Published: 10 January 2013

Abstract: Vitamin D, the sunshine vitamin, has been made on earth for at least 750 million years. Vitamin D evolved during this time into a hormone not only for regulating calcium and bone metabolism, but also for a variety of noncalcemic actions that have been related to decreasing risk of common cancers, autoimmune diseases, infectious diseases and heart disease. Vitamin D requires hydroxylations in the liver and kidneys to be activated to 1,25-dihydroxyvitamin D [1,25(OH)2D]. 1,25(OH)2D interacts with its vitamin D receptor in target tissues to enhance intestinal calcium absorption, mobilize calcium from the skeleton and have a wide range of other genomic effects. 1,25(OH)2D3 is not only made in the kidneys, but made in many other tissues throughout the body for regulating cell proliferation, decreasing cellular malignancy and controlling the production of as many as 200 different gene products. Vitamin D status is determined by measuring serum 25-hydroxyvitamin D [25(OH)D]. A blood level of 25(OH)D > 30 ng/ml is considered to be vitamin D sufficient, whereas < 20 ng/ml is deficient, and 21-29 is insufficient. Sun exposure is a major source of vitamin D for most humans. In the absence of sun exposure, at least 25 µg (1,000 IU) of vitamin D3 is required to satisfy the body’s requirement.

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