Slow down, enzymes at work

the hormone relied on the sympathetic nervous system, the branch that pumps out adrenaline during emergencies but at other times emits a hormonal trickle to maintain a low level of stimulation. This baseline activity was lower in mice lacking the leptin receptor, indicating a connection between leptin and the sympathetic nervous system. When that connection was broken by deleting the adrenaline receptor from mice osteoblasts, insulin levels shot up. The researchers then dosed mice with a sympathetic stimulator. Rodents lacking leptin or the adrenaline receptor on their osteoblasts turned out normal amounts of osteocalcin, but much of it was in an inert form. That result suggests leptin affects insulin release by indirectly inactivating osteocalcin. The work boosts researchers’ hopes of using osteocalcin to treat diabetes—a possibility some drug companies have already started to investigate. Hinoi, E., et al. 2008. J. Cell Biol. doi:10.1083/jcb.200809113.