Berry Thomas M, Moustafa Ahmed A
School of Psychology, Western Sydney University, Sydney, New South Wales, Australia.
School of Psychology, Western Sydney University, Sydney, New South Wales, Australia; Marcs Institute for Brain and Behaviour, Western Sydney University, Sydney, New South Wales, Australia; Department of Human Anatomy and Physiology, The Faculty of Health Sciences, University of Johannesburg, South Africa.
Clin Nutr ESPEN. 2021 Jun;43:191-196. doi: 10.1016/j.clnesp.2021.02.023. Epub 2021 Mar 16.
BACKGROUND & AIMS: In this article we connect the dysregulation of the transsulfuration pathway to bone dysregulations and propose a novel treatment for osteoporosis. Current treatments for osteoporosis are very frequently inadequate. In osteoporosis, the risk of fractures increases with increased homocysteine (Hcy).
Here, we conduct a review on the relationship between osteoporosis and the dysregulation of the transsulfuration pathway.
we show that the transsulfuration pathway metabolizes Hcy to L-cysteine. Increased Hcy levels point to the transsulfuration pathway being dysregulated. With the transsulfuration pathway dysregulated, there will be decreased levels of L-cysteine and decreased levels of taurine, which is synthesized from L-cysteine. Taurine levels are decreased in patients with osteoporosis. Taurine regulates intracellular calcium homeostasis. Taurine, also, when conjugated with bile acids assists with absorption of fats and fat-soluble vitamins such as vitamin D and vitamin K. Dysregulated calcium homeostasis, decreased calcium absorption and decreased absorption of vitamin D and vitamin K due to low levels of taurine negatively affect bone mineral density (BMD) leading to osteoporosis and fractures.
In this article, we propose that a combination of taurine, calcium, vitamin D and vitamin K, could increase BMD reducing number of years spent in disability and reducing deaths due to fractures in patients with osteoporosis.
在本文中，我们将转硫途径的失调与骨骼失调联系起来，并提出一种治疗骨质疏松症的新方法。目前治疗骨质疏松症的方法常常效果不佳。在骨质疏松症中，骨折风险会随着同型半胱氨酸（Hcy）水平的升高而增加。
在此，我们对骨质疏松症与转硫途径失调之间的关系进行综述。
我们发现转硫途径将Hcy代谢为L-半胱氨酸。Hcy水平升高表明转硫途径失调。随着转硫途径失调，L-半胱氨酸水平会降低，由L-半胱氨酸合成的牛磺酸水平也会降低。骨质疏松症患者的牛磺酸水平降低。牛磺酸调节细胞内钙稳态。此外，牛磺酸与胆汁酸结合时有助于脂肪以及维生素D和维生素K等脂溶性维生素的吸收。由于牛磺酸水平低导致的钙稳态失调、钙吸收减少以及维生素D和维生素K吸收减少会对骨密度（BMD）产生负面影响，进而导致骨质疏松症和骨折。
在本文中，我们提出牛磺酸、钙、维生素D和维生素K联合使用，可以提高骨密度，减少骨质疏松症患者的残疾时间，并降低因骨折导致的死亡人数。
