ABSTRACT
El cáncer es una de las mayores causas de muerte en el mundo. Si bien la vitamina D (colecalciferol) ha sido asociada a la regulación de la homeostasis de calcio, muchos son los datos epidemiológicos, bioquímicos y genéticos sobre otros efectos importantes de la vitamina D, como el desarrollo y la progresión de diferentes cánceres. El objetivo del presente artículo es revisar distintos aspectos acerca de los mecanismos de acción y efectos moleculares de la vitamina D o sus metabolitos y de los indicadores epidemiológicos que los correlacionan con el cáncer, su prevención y tratamiento. El estudio de los efectos de la vitamina D se ha vuelto muy amplio: nuevos genes, nuevos blancos, mecanismos diferentes. Niveles adecuados de vitamina D son necesarios para una gran cantidad de procesos fisiológicos y no solamente para el mantenimiento de la homeostasis del calcio. Los estudios clínicos podrían revisar las recomendaciones sobre las dosis de vitamina D que puedan proteger también contra el desarrollo del cáncer.
Subject(s)
Humans , Male , Female , Calcitriol/metabolism , Calcitriol/therapeutic use , Vitamin D Deficiency/complications , Vitamin D Deficiency/epidemiology , Neoplasms/prevention & control , Vitamin D , Vitamin D/metabolism , Vitamin D/chemistry , Cell Differentiation , Nutritional StatusABSTRACT
A vitamina D participa (d)o metabolismo mineral e sua deficiência está associada com doenças extra-ósseas Estudos têm evidenciado hipovitaminose Dna população geral e em renais crônicos. Na progressão da doença renal crônica (DRC), a redução dos níveis de calcitriol, hipocalcemia e hiperfosfatemiasão fatores causais do hiperparatireoidismo secundário (HPTS). Utilizamos o calcitriol para o manejo do HPTS e da hipovitaminose D per se também devemser enfatizadas. Novos análogos da vitamina D, desenvolvidos para substituírem o calcitriol devido à hipercalcemia e hiperfosfatemia associadas ao seuuso, não se mostraram superiores no controle do HPTS. O estado de conhecimento atual sugere a realização de estudos randomizados, controlados ecom amostragem maior para comparar efetividade e segurança entre estes análogos e o calcitriol. Assim, estes estudos poderiam sinalizar para um melhor controle mineral e da doença óssea e resultar em um impacto favorável na morbi-mortalidade na DRC.
Vitamin D has been reported as pivotal for mineral metabolism and bone health, and its deficiency has also been associated with non-skeletal diseases.Many studies have shown high prevalence of vitamin D deficiency in general population as well as in chronic kidney disease (CKD) patients. In CKD progression, low calcitriol levels, hypocalcemia and hyperphosphatemia have all been implicated in the genesis of the secondary hyperparathyroidism (SHPT).In addition to calcitriol supplementation for SHPT management, emphasis should be given to the diagnosis and treatment of vitamin deficiency itself. Newvitamin D analogs were developed in an attempt to overcome the hypercalcemia and hyperphosphatemia that can follow calcitriol treatment but currentknowledge does not allow any conclusion about superiority of new analogs. Large randomized controlled trials studies are needed to compare efficacy and safety of these analogs and calcitriol. These studies could promote a better understanding of mineral metabolism and bone disease control, and result in a favorable impact on morbidity and mortality of CKD patients.
Subject(s)
Humans , Calcitriol/analogs & derivatives , Calcitriol/metabolism , Avitaminosis/therapy , Kidney Failure, Chronic/metabolism , Kidney Failure, Chronic/therapy , Vitamin D/analogs & derivatives , Vitamin D/metabolism , Vitamin D/therapeutic useABSTRACT
This work describes the involvement of TRPC proteins in capacitative calcium entry (CCE) induced by 1a,25-dihydroxy-vitamin-D3 [1a,25(OH)2D3] in chick skeletal muscle and in rat osteoblast-like cells (ROS 17/2.8) and the role of the vitamin D receptor (VDR) in this non-genomic rapid response mediated by the hormone. We propose that an endogenous TRPC3 protein mediates 1a,25(OH)2D3 modulation of CCE in these cells, which seems to implicate VDR-TRPC3 association and the participation of an INAD-like scaffold protein.