Health | Innovation | Maternity
How a Brain Hormone Could Protect Nursing Mothers’ Bones
New Research in Mice Reveals Potential Treatment for Osteoporosis by Boosting Bone Regeneration
After birth, estrogen levels, which play a vital role in maintaining bone health, drop significantly. Lactation further drains the skeleton of calcium. Despite these challenges, nursing mothers tend to maintain strong, dense bones.
A recent study in mice suggests that a hormone released from the brain might be the key to this resilience.
The hormone in question, CCN3, may take over the role of enhancing bone stem cell activity when estrogen levels decline after birth. This could lead to increased bone tissue production, according to research published on July 10, 2024, in Nature. The CCN3 hormone originates in the hypothalamus, a brain region that also helps regulate appetite and body temperature.
This discovery not only sheds light on the mystery of strong bones in nursing mothers but could also pave the way for new treatments to heal fractures and combat bone loss in older adults.
Researchers initially noticed that blocking an estrogen receptor in the hypothalamus of female mice resulted in unusually high bone density. The mutant mice displayed a significantly increased number of bone stem cells compared to normal mice, according to stem cell biologist Thomas Ambrosi from the University of California, Davis.
To explore this further, the researchers looked at the role of diet in bone density and hormone production, given the hypothalamus’s role in regulating appetite. They discovered that placing the mutant mice on a high-fat diet returned their bone density to normal levels. By analyzing which bone-strengthening factors were reduced in these mice, the team narrowed down potential candidates to a few, with CCN3 emerging as the most promising.
In laboratory tests, when scientists treated mouse stem cells with CCN3, bits of bone began to form. They also found that CCN3 levels increased in female rats during lactation, suggesting the hormone helps maintain bone strength during breastfeeding, a period when estrogen levels are low.
The research team then tested CCN3 on elderly mice with bone fractures, which are typically slow to heal. Applying a hydrogel patch containing CCN3 to the injury sites stimulated bone formation, leading to faster recovery.
If CCN3 has similar effects on human bone stem cells, it could lead to new treatments for osteoporosis, a condition characterized by weak and brittle bones.
While there are many drugs available to prevent bone loss, options for stimulating sustained bone formation are still limited, says Khosla. Future medications based on CCN3’s tissue-building properties could potentially revolutionize bone regeneration treatments.
