In female individuals, oestradiol preserves bone mass. However, oestradiol levels drop during lactation, which is also a time when calcium is being removed from the maternal bone. How bone mass is maintained in lactating female individuals has been unclear. A study published in Nature has now identified a new mechanism for maintaining bone mass, which involves brain–bone crosstalk.

Next, the researchers conducted single-cell RNA sequencing on osteochondral skeletal stem cells from mutant female mice, which gave limited insights. The observation that a high-fat diet degraded the bone phenotype of the mutant mice enabled Muriel Babey, co-lead on this study, to narrow down the list of potential factors. Of these, CCN3 was found to be present near the third ventricle in female Esr1^Nkx2-1-cre mice, but was absent in the wild-type mice. Furthermore, CCN3 expression correlated well with the appearance of the bone phenotype and was co-localized with KISS1 neurons in the female mutant mice.

在女性个体中，雌二醇可以保留骨量。然而，在哺乳期间，雌二醇水平会下降，这也是钙从母体骨骼中流失的时期。哺乳期女性如何维持骨量尚不清楚。发表在《自然》杂志上的一项研究现已确定了一种维持骨量的新机制，其中涉及脑-骨串扰。

接下来，研究人员对突变雌性小鼠的骨软骨骨骼干细胞进行了单细胞 RNA 测序，但得到的见解有限。观察到高脂肪饮食会降低突变小鼠的骨表型，这项研究的共同领导者 Muriel Babey 缩小了潜在因素的范围。其中，CCN3被发现存在于雌性Esr1 ^Nkx2-1-cre小鼠的第三脑室附近，但在野生型小鼠中不存在。此外，CCN3 表达与骨表型的外观密切相关，并且与雌性突变小鼠中的 KISS1 神经元共定位。