PDF(Pubmed)
Abstract：
The first evidence of the existence of vitamin A was the observation 1881 that a substance present in small amounts in milk was necessary for normal development and life. It was not until more than 100 years later that it was understood that vitamin A acts as a hormone through nuclear receptors. Unlike classical hormones, vitamin A cannot be synthesized by the body but needs to be supplied by the food as retinyl esters in animal products and ß-carotene in vegetables and fruits. Globally, vitamin A deficiency is a huge health problem, but in the industrialized world excess of vitamin A has been suggested to be a risk factor for secondary osteoporosis and enhanced susceptibility to fractures. Preclinical studies unequivocally have shown that increased amounts of vitamin A cause decreased cortical bone mass and weaker bones due to enhanced periosteal bone resorption. Initial clinical studies demonstrated a negative association between intake of vitamin A, as well as serum levels of vitamin A, and bone mass and fracture susceptibility. In some studies, these observations have been confirmed, but in other studies no such associations have been observed. One meta-analysis found that both low and high serum levels of vitamin A were associated with increased relative risk of hip fractures. Another meta-analysis also found that low levels of serum vitamin A increased the risk for hip fracture but could not find any association with high serum levels of vitamin A and hip fracture. It is apparent that more clinical studies, including large numbers of incident fractures, are needed to determine which levels of vitamin A that are harmful or beneficial for bone mass and fracture. It is the aim of the present review to describe how vitamin A was discovered and how vitamin A is absorbed, metabolized and is acting as a ligand for nuclear receptors. The effects by vitamin A in preclinical studies are summarized and the clinical investigations studying the effect by vitamin A on bone mass and fracture susceptibility are discussed in detail.
摘要：
维生素A存在的第一个证据是1881年的观察，即牛奶中少量存在的物质是正常发育和生活所必需的。直到100多年后，人们才知道维生素A通过核受体充当激素。不像经典的荷尔蒙,维生素A不能由人体合成，但需要由食品作为动物产品中的视黄醇酯和蔬菜和水果中的β-胡萝卜素提供。全球范围内,维生素A缺乏是一个巨大的健康问题，但是在工业化国家，过量的维生素A被认为是继发性骨质疏松症和骨折易感性增加的危险因素。临床前研究明确表明，由于骨膜骨吸收增强，维生素A的含量增加会导致皮质骨量减少和骨骼变弱。最初的临床研究表明，维生素A的摄入量之间存在负相关，以及维生素A的血清水平,骨质量和骨折敏感性。在一些研究中,这些观察已经得到证实，但在其他研究中没有观察到这种关联.一项荟萃分析发现，低和高血清维生素A水平与髋部骨折的相对风险增加有关。另一项荟萃分析还发现，低水平的血清维生素A会增加髋部骨折的风险，但找不到与高水平的血清维生素A和髋部骨折的任何关联。很明显，更多的临床研究，包括大量的意外骨折，需要确定哪些维生素A水平对骨骼质量和骨折有害或有益。本综述的目的是描述维生素A是如何被发现的，以及维生素A是如何被吸收的。代谢并作为核受体的配体。总结了维生素A在临床前研究中的作用，并详细讨论了研究维生素A对骨量和骨折敏感性的影响的临床研究。
