Prior Jerilynn C
Endocrinology and Metabolism, Centre for Menstrual Cycle and Ovulation Research, University of British Columbia, Vancouver Coastal Health Research Institute, Vancouver V5Z 1M9, Canada.
Trends Mol Med. 2007 Jan;13(1):1-3. doi: 10.1016/j.molmed.2006.11.004. Epub 2006 Dec 1.
For many years, osteoporosis in women was equated with estrogen deficiency. The recent articles by Zaidi and colleagues offer a new challenge to the estrogen-deficiency-osteoporosis hypothesis by showing that follicle-stimulating hormone (FSH) stimulates osteoclastic bone resorption perhaps through tumor necrosis factor-alpha (TNF-alpha). These authors, however, neglected to mention bone abnormalities and high testosterone levels that were previously shown in FSH-receptor knockout and other modified mice. It is also possible that they have overemphasized potential relationships of these new data with human bone loss. Despite these fascinating data, the paradigm of FSH causing hypogonadal bone loss is not yet ready to displace the estrogen-deficiency-osteoporosis paradigm, although that model already faces considerable challenge.
多年来,女性骨质疏松症一直被等同于雌激素缺乏。扎伊迪及其同事最近发表的文章对雌激素缺乏导致骨质疏松症的假说提出了新挑战,他们指出促卵泡激素(FSH)可能通过肿瘤坏死因子-α(TNF-α)刺激破骨细胞的骨吸收。然而,这些作者忽略提及先前在FSH受体基因敲除小鼠和其他基因改造小鼠中发现的骨骼异常和高睾酮水平。他们也有可能过度强调了这些新数据与人类骨质流失的潜在关系。尽管有这些引人入胜的数据,但FSH导致性腺功能减退性骨质流失的范例尚未准备好取代雌激素缺乏导致骨质疏松症的范例,尽管后者已经面临相当大的挑战。