Mice that lack either leptin or its receptor protein for genetic reasons are obese and also have small, poorly developed, ovaries or testes. Heavier, denser bones can now be added to these other symptoms of leptin deficiency. Throughout life, your bones are constantly broken down and rebuilt. Even though bone seems such a permanent material, it constantly undergoes remodelling and renewal, which is why it can repair itself. Existing bone is broken down or 'resorbed' by one set of cells, and new bone is produced by another.
Growth stops after puberty, but bone resorption and production continue, balancing each other out.
After the menopause in women, however, bone resorption can become predominant, leading to osteoporosis, in which bones become weak and are easily broken. Given the strong connection between the decline in ovarian function at menopause and the onset of osteoporosis, Ducy and her team thought that the obese mice would have weaker bones than normal. But, to their surprise, exactly the opposite turned out to be the case. To confirm that the greater bone mass in the obese mice was caused specifically by the lack of leptin, they measured the levels of other hormones known to influence bone growth and found them normal. They could also detect increased bone mass long before the obsesity developed, so they could rule out the possibility that it was simply a secondary effect of obesity.