雌激素和骨骼关系的最新进展

在70多年前发表的1篇有巨大影响的论文中,FullerAlbright"观察了42例65岁及以下‘特发性'骨质疏松患者.40例为绝经后女性,2例为男性.虽然数名绝经前年龄的妇女中也出现了这类骨质疏松,但是这几名妇女均经过外科手术造成了绝经.     

雌激素和骨骼关系的最新进展

在70多年前发表的1篇有巨大影响的论文中,FullerAlbright"观察了42例65岁及以下‘特发性'骨质疏松患者.40例为绝经后女性,2例为男性.虽然数名绝经前年龄的妇女中也出现了这类骨质疏松,但是这几名妇女均经过外科手术造成了绝经.     

雌激素和大肠癌关系的研究进展

大肠癌是临床上常见的恶性肿瘤,近年来其发病率及死亡率在我国都呈上升趋势.自20世纪80年代有研究认为使用外源性的雌激素可降低妇女结肠癌的发病率后,人们对雌激素的使用与结肠癌发病率的相关性进行了较多研究.本文就雌激素和结肠癌关系研究进展进行综述.     

雌激素和雌激素受体基因多态性与骨代谢异常的关系

骨质疏松是一种基因调控的疾病，以骨量减少和骨的微观结构退化为特征，雌激素和雌激素受体基因多态性是其重要影响因素之一。雌激素与受体结合后，调节成骨细胞破骨细胞的骨形成和骨吸收作用，而雌激素受体基因多态性则被认为与骨矿物质密度（ＢＭＤ）呈密切相关，尤其对绝经前妇女和男性的ＢＭＤ起到了预测因子的作用。     

雌激素和雌激素受体基因多态性与骨代谢异常的关系

骨质疏松是一种多基因调控的疾病 ,以骨量减少和骨的微观结构退化为特征 ,雌激素和雌激素受体基因多态性是其重要影响因素之一。雌激素与受体结合后 ,调节成骨细胞和破骨细胞的骨形成和骨吸收作用 ,而雌激素受体基因多态性则被认为与骨矿物质密度 (BMD)呈密切相关 ,尤其对绝经前妇女和男性的BMD起到了预测因子的作用     

鹌鹑血清雌激素和动脉壁雌激素受体与动脉粥样硬化的关系

高脂对平滑肌细胞异常ＨＬＡ－ＤＲ抗原表达的影响王淑华，胡京红，卢泳才（北京中医药大学北京，１０００２９）近年来的研究发现，体外培养的血管内皮细胞和平滑肌细胞（ＳＭＣ）加入ｒ－ＩＮＦ后可使正常情况下不呈ＤＲ表达的细胞呈ＤＲ表达。我们的研究亦已证明：以人...     

鹌鹑血清雌激素和动脉壁雌激素受体与动脉粥样硬化的关系

鹌鹑血清雌激素和动脉壁雌激素受体与动脉粥样硬化的关系张冰，卢泳才，贾褚东，周玉琳（北京中医药大学，北京１０００２９）世激素（ｓｅｘｕａｌｈｏｒｍｏｍｏｎｅ，ＳＨ）水平异常改变作为冠心病（ｃｏｒｏｎａｒｙｈｅａｒｔｄｉｓｅａｓｅ，ＣＨＤ）的易患因子，早...     

一氧化氮和雌激素的关系在心血管病中的研究进展

美国每年有 5 0万妇女死于心血管疾病 ,是美国妇女死亡的第一位原因。心血管疾病的表现在男性和女性之间有明显差别 :男性一生中发生冠心病的危险性要比女性高 3.5倍。“Framingham研究”证实了在年龄上有特异性差别 :在 2 0岁至 30岁期间 ,女性与男性发生冠心病的危险性比值为 1:7,随后这一比值逐渐降低 ,到 70岁以后达到男女相等。冠心病危险性的这种逐步上升在绝经后比较明显 ;最近有人估计 ,绝经可直接使危险性增加 3倍 [1] 。尽管在绝经后性别间的差别消失 ,但就整体而言 ,妇女发生冠心病仍然比较少。在冠心病的发病上 ,她们比男性晚 …     

miRNA与心房颤动关系的最新进展

微小核糖核酸(miRNA)是一类内生的长度为19～24个核苷酸的单链非编码RNA。它通过调节靶目标信使核糖核酸(mRNA)的降解和翻译,指导RNA诱导沉默复合体调节靶基因表达,在细胞生理过程中发挥重要作用,是转录后水平调控基因表达的重要分子。目前miRNA与心血管疾病之间的关系在国内外也成为研究的热点,现选取相关miRNA与心血管疾病中心房颤动的电重构与结构重构之间的关系做一综述。     

雌激素与内皮祖细胞的关系

近年来,对雌激素的研究趋于全面,雌激素与内皮祖细胞(endothelial progenitor cells,EPC)关系的研究也日渐增多.目前,对雌激素与EPC的综述,主要论述雌激素对EPC的增殖、分化等作用,并未讨论雌激素其他方面的效应.本文从多个方面讨论雌激素与EPC之间的关系,除了增加EPC动员、增殖、分化等作用之外,也着力讨论了雌激素的其他作用.因此本文主要总结雌激素在不同情况下表现出的不同作用及推测其作用机制.     

Increased PTHrP and decreased estrogens alter bone turnover but do not reproduce the full effects of lactation on the skeleton

During lactation, calcium is mobilized from the maternal skeleton to supply the breast for milk production. This results in rapid but fully reversible bone loss. Prior studies have suggested that PTHrP, secreted from the breast, and estrogen deficiency, due to suckling-induced central hypogonadism, combine to trigger bone resorption. To determine whether this combination was sufficient to explain bone loss during lactation, we raised PTHrP levels and decreased levels of estrogens in nulliparous mice. PTHrP was infused via osmotic minipumps and estrogens were decreased either by using leuprolide, a long-acting GnRH agonist, or by surgical ovariectomy (OVX). Bone mineral density declined by 23.2 ± 1.3% in the spine and 16.8 ± 1.9% in the femur over 10 d of lactation. This was accompanied by changes in trabecular architecture and an increase in both osteoblast and osteoclast numbers. OVX and PTHrP infusion both induced a modest decline in bone mineral density over 10 d, but leuprolide treatment did not. The combination of OVX and PTHrP was more effective than either treatment alone, but there was no interaction between PTHrP and leuprolide. None of the treatments reproduced the same degree of bone loss caused by lactation. However, both forms of estrogen deficiency led to an increase in osteoclasts, whereas infusion of PTHrP increased both osteoblasts and osteoclasts. Therefore, although the combination of PTHrP and estrogen deficiency contributes to bone loss, it is insufficient to reproduce the full response of the skeleton to lactation, suggesting that other factors also regulate bone metabolism during this period.     

Androgens and the skeleton

Loss of estrogens or androgens causes bone loss by increasing the rate of bone remodeling, and also causes an imbalance between resorption and formation by prolonging the lifespan of osteoclasts and shortening the lifespan of osteoblasts. Conversely, treatment with androgens, as well as estrogens, maintains cancellous bone mass and integrity, regardless of age or sex. Both androgens, via the androgen receptor (AR), and estrogens, via the estrogen receptors (ERs) can exert these effects, but the relative contribution of these 2 pathways remains uncertain. Androgens, like estrogens, stimulate endochondral bone formation at the start of puberty, whereas they induce epiphyseal closure at the end of puberty, thus, they have a biphasic effect. Androgen action on the growth plate is, however, clearly mediated via aromatization into estrogens and interaction with ER alpha. Androgens increase, while estrogens decrease radial growth. This differential effect of the sex steroids may be important because bone strength in males seems to be determined by higher periosteal bone formation and, therefore, greater bone dimensions. Experiments in mice suggest that both the AR and ER alpha pathways are involved in androgen action on radial bone growth. ER beta may mediate growth-limiting effects of estrogens in the female but does not seem to be involved in the regulation of bone size in males. In conclusion, androgens may protect men against osteoporosis via maintenance of cancellous bone mass and expansion of cortical bone. This androgen action on bone is mediated by the AR and ER alpha.