Breastfeeding Strains Bones, But a Brain Hormone May Protect
Giving birth and caring for a newborn can be tough on a mother’s bones. Estrogen, which regulates bone growth, drops sharply after birth, and lactation depletes calcium from the skeleton. However, nursing mothers still maintain strong, dense bones. A study in mice suggests a brain-released hormone might be the reason.
Researchers report in Nature on July 10 that when estrogen levels fall post-birth, the hormone CCN3 may boost bone stem cell activity, enhancing tissue production.
This hormone, originating in the hypothalamus, which regulates appetite and body temperature, could explain nursing mothers’ strong bones. It might also offer new ways to heal fractures and combat bone loss in old age.
The study “identifies a new direct loop between the hypothalamus and bone, which is, I think, totally unexpected,” says Sundeep Khosla, a bone researcher at the Mayo Clinic in Rochester, Minn., who was not involved in the study.
Uncovering the Link Between Hypothalamus and Bone Density in Mutant Mice
Researchers investigated why blocking an estrogen receptor in the hypothalamus caused female mice to develop exceptionally high bone density. Stem cell biologist Thomas Ambrosi of the University of California, Davis, notes that these mutant mice had a significantly increased number of bone stem cells compared to normal mice.
Given the hypothalamus’s role in appetite regulation, researchers examined the impact of diet on bone density and hormone production. They discovered that placing mutant mice on a high-fat diet restored their bone density to normal levels.
Analyzing which bone-strengthening factors decreased in these mice helped narrow potential candidates from hundreds to a few, says Muriel Babey, an endocrinologist at the University of California, San Francisco.
CCN3’s Role in Bone Formation and Maternal Strength During Lactation
Adding these substances to mouse stem cells in a petri dish revealed that CCN3 promoted bone formation. The team also found that CCN3 levels spiked in female rats during lactation, indicating CCN3’s role in maintaining maternal bone strength when estrogen levels drop.
Ambrosi’s team then tested CCN3 in elderly mice with bone fractures, which usually heal poorly. Applying a hydrogel patch with the hormone to injury sites stimulated bone formation and sped up recovery. If CCN3 has similar effects on human skeletal stem cells, it could lead to new osteoporosis treatments.
Although there are many drugs to prevent bone loss, Khosla notes, “we’re still limited in terms of the drugs that stimulate bone formation, and particularly do it in a sustained way — not just for months, but over years.” Due to CCN3’s tissue-building properties, future drugs based on this hormone could potentially enhance bone regeneration.
The study “highlights how much important biology and physiology is happening during reproductive life stages,” says coauthor William Krause, a pharmacologist also at UC San Francisco. “There’s potentially a lot of biology there that remains to be covered.”
Read the original article on: Science News
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