UT Southwestern researchers, working with colleagues in Japan, now have found that mice lacking orexins also have very thin and fragile bones that break easily because they have fewer cells called osteoblasts, which are responsible for building bones.Oh yeah, that explains a whole lot of periodontitis and arterial calcification now doesn't it....
Orexins seem to play a dual role in the process: they both promote and block bone formation. On the bones themselves, orexins interact with another protein, orexin receptor 1 (OX1R), which decreases the levels of the hunger hormone ghrelin. This slows down the production of new osteoblasts and, therefore, blocks bone formation locally. At the same time, orexins interact with orexin receptor 2 (OX2R) in the brain. In this case, the interaction reduces the circulating levels of leptin, a hormone known to decrease bone mass, and thereby promotes bone formation. Therefore, osteoporosis prevention and treatment may be achieved by either inhibiting OX1R or activating OX2R.
"We were very intrigued by this yin-yang-style dual regulation," said Dr. Wan, a member of the Cecil H. and Ida Green Center for Reproductive Biology Sciences and UT Southwestern's Harold C. Simmons Comprehensive Cancer Center. "It is remarkable that orexins manage to regulate bone formation by using two different receptors located in two different tissues."
abstract
(update- if increasing orexin levels is the goal, then reducing carb intake is the solution. I'm taking the "no way in hell they will advocate that" bet.)
