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Skeleton regulates male fertility

Exciting revelations on your framework

There are many things without which we could not live. They vary from person to person but one of our ‘essentials’ that no one could live without is definitely the skeleton.

It enables movement, supports muscles, protects our vital organs and acts as ion storage, to name just a few of its functions. It should not be surprising that many scientists were and still are fascinated by the human ‘frame’. What can surprise us, however, is how many facts were discovered very recently or still have to be discovered.

One of the very recent (and quite surprising) discoveries regarding bones is that osteocalcin, a hormone produced in bones which regulates bone regeneration affects male fertility. Experiments carried out on mice showed that osteocalcin increases testosterone production in testis and that this hormone is necessary for proper functioning of male reproductive system.

Until now scientists were aware of the effect of sex hormones (oestrogen in female and testosterone in male) on bone growth, regeneration and mass. They noticed that when oestrogen is not produced anymore in menopausal women, their bone mass decreases and increased risk of osteoporosis is observed.

Having in mind that communication between two organs is rarely unilateral scientists asked themselves if the skeleton could also affect gonads. Since the observed effect of oestrogen on bones was very significant, they hypothesised that the opposite dependence is much stronger in females than in males. Experiments showed however, that bones in fact regulate fertility but only in males.

When osteocalcin was added to Leydig cells (cells in testis responsible for testosterone production) their testosterone production increased significantly. Osteocalcin injection into male mice resulted in higher blood testosterone level. Adding osteocalcin did not affect however the production of oestrogen in ovaries.

Genetically modified male individuals that did not produce osteocalcin were less fertile than wild type. Those mutants had much lower blood testosterone level, smaller testis and less sperm than normal individuals. Genetically modified females however had no changes in oestrogen level or gonad’s structure and morphology.

The key molecule providing clarification for the fact that osteocalcin regulates fertility in males but not in females is Gprc6a, a G Protein-Coupled Receptor. It is found on the surface of Leydig cells and transduces signal emitted by osteocalcin leading to increased testosterone production. It is not present in follicular cells of ovaries what explains why female fertility is not affected by osteocalcin.

It seems like the mechanism in people can be similar to this observed in mice. Our bones also produce osteocalcin and most of the endocrine systems function almost identically in humans and in mice. If osteocalcin-testosterone interaction is also the case it might explain many cases of unfertile men and could become a target for infertility treatment.

It was relatively recently that the bones were considered as a very rigid and inflexible structure, nothing more than accumulation of calcium and proteins. Only past ten years revealed the dynamic nature of bones and very important role they play in controlling and regulating physiological processes. How are bones going to surprise us next time?

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