Higher iron levels after menopause appear to be risk factors for osteoporosis, and hormone hepcidin, which regulates iron, might be a potential therapeutic target for this condition.
In the study, researchers applied genetic modification techniques to alter the production of endogenous hormone hepcidin in a mouse model, aiming to affect the iron levels in the body. Making use of both knockout and overexpression murine models, researchers focused specifically on the correlational aspects of hepcidin levels and bone loss. Further to that, the impact of iron overload on reactive oxygen species (ROS) activity was tested, as well as its effect on the slowed down work of primary osteoblasts.
On the other hand, the effect of iron depletion was observed, presented as the reversed phenomenon through inhibiting the functions of the primary osteoclasts. Through this work, researchers investigated how iron accumulation interferes with general bone health in postmenopausal conditions. They further verified the 'Huang's hypothesis' - proposed in previous studies - about the potential therapeutic value of hepcidin for postmenopausal osteoporosis.
