A brain estrogen signal helped regulate bone mass in female mice
In experiments, female mice with one estrogen signal disabled in selected brain cells had greater bone mass at 16 weeks than littermate controls.
Our read
Mechanisms- Studied:
- Experiments in gonadal-intact female mice, against littermate control mice (Funded by the product's maker)
- What changed:
- Female mice lacking membrane estrogen signaling in POMC neurons had higher femur bone mass than controls
- The catch:
- Higher circulating estrogen could explain cortical bone gains in intact mutant females
- In the record:
- One of 517 papers on ESR1 on record: 37 with results in people, 59 in animals.
Editor of record: Boris Djordjevic · AgingResearch.News
Female mice with an estrogen signal genetically disabled in selected nerve cells in the hypothalamus, a brain region that helps regulate hormones, had more bone in an animal experiment. The alteration targeted estrogen receptor alpha, a protein that senses estrogen, specifically its signaling at the cell surface. At 16 weeks, mice with intact ovaries had altered sex hormone levels and more of both the hard outer bone and spongy inner bone than littermate controls.
In a separate experiment, females had their ovaries removed at 16 weeks. After one week, groups of 10–12 mice received daily injections of estradiol, an estrogen, at 1 or 6 micrograms per mouse, or the carrier fluid alone, for three weeks. Altered mice showed a greater spongy-bone response in the thighbone, but a similar outer-bone response. Males whose testes had been removed showed estrogen responses similar to controls.
Why it matters
Bone maintenance is central to questions about bone loss with age. This work examined how the brain contributes to that control through estrogen signaling.
Caveats
The estrogen experiments used mice with ovaries or testes removed, rather than animals undergoing natural aging. The results do not show whether changing this signal would prevent fractures in older people.
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