The problem turned out to be a mutation that inactivated a gene called LRP5.
这个问题产生于导致LRP5基因活动受阻的变异。
The more LRP5, the more the enzyme is blocked, and the less serotonin is made.
LRP5越多，越多的酶被阻滞，复合胺产生越少。
The human skeleton is affected by mutations in low-density lipoprotein receptor-related protein 5 (LRP5).
低密度脂蛋白受体相关蛋白5 (LRP5)基因突变可影响人体骨骼。
After 6 weeks of implantation, the implant bone contact rate and bone density in the LV-LRP5 group were lower than those in the blank group.
种植体植入6周后，空白组种植体与新骨之间的接触较广泛，而LV- LRP5组种植体与新骨之间的接触较局限。
Osteoporosis researchers jumped on these findings, realizing LRP5 could hold clues to the disease. But most assumed that LRP5's role was in bone itself.
骨质疏松研究者对这些发现做了更深入的研究，明确了LRP5与骨质疏松紧密相关。但大多数假定LRP5的作用在骨头本身。
A few years later, another mutation was found in LRP5 that produced the opposite effect, extremely dense bones and resistance to osteoporosis. In this case, LRP5 was overactive.
几年后，LRP5基因的另一个变异被发现能相反的作用，即骨密度异常高和抵抗骨质疏松，在这种情况下，LRP5基因过于活跃。
Conclusion Q89R polymorphism in LRP5 gene may have an influence on BMD in postmenopausal women, which suggests that LRP5 gene is a candidate for the genetic determination of BMD.
结论LRP5基因Q 89r多态性位点可能对绝经后妇女骨密度有影响，提示LRP5基因是影响骨密度的候选基因之一。
To understand how Lrp5 influences bone properties, we generated mice with osteocyte-specific expression of inducible Lrp5 mutations that cause high and low bone mass phenotypes in humans.
为了研究Lrp5如何影响骨特性，我们建立了骨细胞特异性表达诱导型Lrp5基因突变的小鼠，该基因突变可导致人类高和低骨量表型。
Objective To investigate the association of lipoprotein receptor-related protein 5(LRP5) gene Q89R, A1330V polymorphism with bone mineral density(BMD) in premenopausal Northern Chinese women.
目的探讨中国北方绝经前妇女低密度脂蛋白受体相关蛋白5（LRP5）基因Q89R、A1330V多态性与骨密度关系。
Objective To investigate the association of lipoprotein receptor-related protein 5(LRP5) gene Q89R, A1330V polymorphism with bone mineral density(BMD) in premenopausal Northern Chinese women.
目的探讨中国北方绝经前妇女低密度脂蛋白受体相关蛋白5（LRP5）基因Q89R、A1330V多态性与骨密度关系。
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