Acción de la vitamina K sobre la salud ósea / Action of vitamin K on bone health

Objetivos: Se admite hoy en día que la vitamina K tiene un papel importante en la salud ósea. Es necesaria para la gamma-carboxilación de la osteocalcina (la proteína no colágena más importante en el hueso), consiguiendo que la osteocalcina funcione. Hay dos formas importantes de la vitamina K (vitamina K1 y vitamina K2), que provienen de diferentes fuentes y tienen diferentes actividades biológicas. Estudios epidemiológicos sugieren que una dieta con niveles altos de vitamina K se asocia con un menor riesgo de fracturas de cadera en hombres ancianos y mujeres. Sin embargo, ensayos clínicos controlados y aleatorizados, realizados con suplementos de vitamina K1 o K2 en la población blanca, no muestran un aumento en la densidad mineral ósea (DMO) en la mayoría de las diferentes partes del esqueleto. Los suplementos con vitamina K1 y K2 pueden reducir el riesgo de fractura, pero los ensayos clínicos que incluyen las fracturas como resultado final tienen limitaciones metodológicas, por lo que se necesitarían ensayos clínicos con mayor número de pacientes y mejor diseñados para comprobar la eficacia de la vitamina K1 y K2 en las fracturas. Como conclusión, podríamos decir que actualmente no existe una evidencia suficiente para recomendar el uso rutinario de suplementos de vitamina K para la prevención de la osteoporosis y las fracturas en mujeres postmenopáusicas (AU)

Objetives: Nowadays it is recognised that vitamin K plays an important role in bone health. It is necessary for the gamma-carboxylation of osteocalcin (the most important non-collagen protein in the bone), making the osteocalcin function. There are two important forms of vitamin K (vitamin K1 and vitamin K2), which come from different sources and have different biological activity. Epidemiological studies suggest that a diet with high levels of vitamin K is associated with a lower risk of hip fractures in older men and in women. However, controlled randomised clinical trials, carried out with supplements of vitamin K1 or K2 in the white population do not show an increase in bone mineral density (BMD) in most of the different areas of the skeleton. Supplementation with vitamin K1 and K2 may reduce the risk of fracture, but the clinical trials which include fractures as a final result have methodological limitations, so clinical trials with greater numbers of patients, and which are better designed, would be needed in order to prove the efficacy of vitamin K1 and K2 in relation to fractures. In conclusion, we may say that there is currently insufficient evidence to recommend the routine use of vitamin K for the prevention of osteoporosis and fractures in postmenopausal women (AU)

[Effect of glucose and bone metabolism in endocrinal disorder].

It is well known that endocrine disorders; glucocorticoid excess including Cushing syndrome, high dose or long term steroid therapy and hyperthyroidism, induce secondary osteoporosis. These common endocrinal disorders affect not only bone metabolism but also glucose metabolism. Glucose metabolisms also play a important role in the progression of osteoporosis. To prevent secondary osteoporosis, multifocal intervention such as correction of insulin resistance or glucose metabolism, lifestyle, and drug therapy, need to be added to current management of endocrinal system.

Vitamin D receptor activators can protect against vascular calcification.

An apparent conflict exists between observational studies that suggest that vitamin D receptor (VDR) activators provide a survival advantage for patients with ESRD and other studies that suggest that they cause vascular calcification. In an effort to explain this discrepancy, we studied the effects of the VDR activators calcitriol and paricalcitol on aortic calcification in a mouse model of chronic kidney disease (CKD)-stimulated atherosclerotic cardiovascular mineralization. At dosages sufficient to correct secondary hyperparathyroidism, calcitriol and paricalcitol were protective against aortic calcification, but higher dosages stimulated aortic calcification. At protective dosages, the VDR activators reduced osteoblastic gene expression in the aorta, which is normally increased in CKD, perhaps explaining this inhibition of aortic calcification. Interpreting the results obtained using this model, however, is complicated by the adynamic bone disorder; both calcitriol and paricalcitol stimulated osteoblast surfaces and rates of bone formation. Therefore, the skeletal actions of the VDR activators may have contributed to their protection against aortic calcification. We conclude that low, clinically relevant dosages of calcitriol and paricalcitol may protect against CKD-stimulated vascular calcification.