Lack of oestrogen is considered to be the main reason for postmenopausal osteoporosis. However, some studies have also proposed that iron accumulation can accelerate osteoporosis after menopause.

Hepcidin is an endogenous hormone which regulates iron in the body. Zhang et al. genetically modified expression of hepcidin, with the aim of modulating iron status in a mouse model. They monitored any effects on bone loss in the mice. Results showed that hepcidin levels were negatively correlated with bone loss.

These results are further evidence of the ‘iron accumulation’ hypothesis, which suggests that high iron levels are risk factors for osteoporosis, and highlight hepcidin as a potential drug target for prevention of postmenopausal osteoporosis.

Read the full article in Journal of Molecular Endocrinology 60 299–308.