New neural hormone protects maternal bones from fractures.
Breast milk contains a lot of calcium, and this calcium is taken from the mother’s bones. Bones should lose mass and density, and therefore become more fragile. Indeed, some young mothers who breastfeed have more bone damage, but only some. That is, the body somehow maintains bone strength during this period, despite the outflow of calcium.
There are several hormones that regulate bone growth to some extent. Estrogen is one of the main ones: it actively stimulates bone tissue development, both in women and men. Increased fragility and brittleness of bones in older women is associated with the drop in estrogen during menopause. However, after childbirth, estrogen levels also decrease, and quite significantly. Then they are restored, but during breastfeeding, it is clearly not estrogen that protects the mother’s bones.
What exactly protects them is written in Nature employees of the University of California, San Francisco. This is a protein called CCN3, or intercellular communication factor 3. It can be called new in the sense that although its existence was known before, its functions remained almost unstudied. CCN3 is synthesized by a group of neurons called Kiss1, located in the arcuate nucleus of the brainstem – several years ago it was discovered that they are involved in reproduction and that they simultaneously depend on bone growth, and only in females. These neurons have receptors for estrogen, and when their estrogen receptors were turned off, the bones became especially dense. New experiments with mice have shown that when Kiss1 neurons stop sensing estrogen, they secrete the aforementioned CCN3 factor.
If CCN3 activity was suppressed in females before pregnancy, their bones lost a lot of mass. (Disabling CCN3 in mothers also affected their offspring: the babies lagged in development and died more often.) In normal mice, without any genetic modifications, the level of CCN3 increased before they began to feed the mice with milk and decreased when they stopped feeding with milk. In general, it can be said that the hormone CCN3 and the neurons that synthesize it protect maternal bones from fractures. It is clear why Kiss1 neurons need estrogen receptors: when the level of estrogen drops after childbirth, this becomes a signal for neurons to actively synthesize bone-preserving CCN3. Most likely, a similar mechanism works in humans, although the human hormone may have its own characteristics.
But CCN3 may not only be useful to young mothers. Although Kiss1 neurons have been shown to work to preserve bone only in females, the CCN3 hormone itself works in both males and females. By regularly injecting it into males and females without cubs, the researchers saw significant increases in bone mass in both. What’s more, when older males with fractures were given a CCN3-laced patch, the bones healed much faster. Similarly, CCN3 strengthened the bones of females who had had their ovaries removed, which left them with little estrogen.
True, questions remain about how exactly CCN3 works, how exactly neurons switch to its synthesis, and how exactly bone cells sense it. When the answers to these questions become known, it will be possible to think about making a medicine based on CCN3 or CCN3-suborbital protein that would save the elderly and not only the elderly from osteoporosis and other diseases that make bones too fragile.
Source: www.nkj.ru
