As a necessary trace element, iron is involved in many physiological processes. Clinical and basic studies have found that disturbances in iron metabolism, especially iron overload, might lead to bone loss and even be involved in postmenopausal osteoporosis. Hepcidin is a key regulator of iron homeostasis. However, the exact role of hepcidin in bone metabolism and the underlying mechanism remain unknown. In this study, we found that in postmenopausal osteoporosis cohort, the concentration of hepcidin in the serum was significantly reduced and positively correlated with bone mineral density. Ovariectomized (OVX) mice were then used to construct an osteoporosis model. Hepcidin overexpression in these mice significantly improved bone mass and rescued the phenotype of bone loss. Additionally, overexpression of hepcidin in OVX mice greatly reduced the number and differentiation of osteoclasts in vivo and in vitro . This study found that overexpression of hepcidin significantly inhibited ROS production, mitochondrial biogenesis, and PGC-1β expression. These data showed that hepcidin protected osteoporosis by reducing iron levels in bone tissue, and in conjunction with PGC-1β, reduced ROS production and the number of mitochondria, thus inhibiting osteoclast differentiation and bone absorption. Hepcidin could provide new targets for the clinical treatment of postmenopausal osteoporosis.

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Background Bone mineral density (BMD) and prevalence of osteoporosis may differ between urban and rural populations. This study aimed to investigate the differences in BMD characteristics between urban and rural populations in Jiangsu, China. Methods A total of 2,711 participants aged 20 years and older were included in the cross-sectional study. Multistage and stratified cluster random sampling was used as the sampling strategy. BMD was measured by the method of dual-energy x-ray absorptiometry (DXA). Data were collected through questionnaires/interview. BMD values at the lumbar spine (L1-L4), femoral neck, total hip, and greater trochanter were collected. Descriptive statistics were used to demonstrate the characteristics of urban and rural participants. Multivariate logistic regression analysis was utilized to analyze the factors that may be associated with osteoporosis in urban and rural populations. Results Of these participants, 1,540 (50.49%) were females and 1,363 (42.14%) were from urban. The prevalence of osteoporosis in urban and rural populations was 5.52% and 10.33%, respectively. In terms of gender, the prevalence of osteoporosis was 2.68% in males and 13.82% in females. For menopausal status, the prevalence of osteoporosis was 30.34% in postmenopausal females and 4.78% in premenopausal females. In urban populations, older age [adjusted odds ratio (AOR) = 2.36, 95%CI, 2.35–2.36), hypertension (AOR = 1.37, 95%CI, 1.36–1.37), unmarried (AOR = 4.04, 95%CI, 3.99–4.09), smoking everyday (AOR = 2.26, 95%CI, 2.23–2.28), family history of osteoporosis (AOR = 1.66, 95%CI, 1.65–1.67), dyslipidemia (AOR = 1.05, 95%CI, 1.04–1.05), and higher β-crosslaps (β-CTX) level (AOR = 1.02, 95%CI, 1.02–1.02) were associated with an increased risk of osteoporosis, while males (AOR = 0.04, 95%CI, 0.04–0.04), higher education level (AOR = 0.95, 95%CI, 0.95–0.95), and aquatic product intake (AOR = 0.99, 95%CI, 0.99–0.99) were related to decreased risk of osteoporosis. Similar results were also observed in rural populations, and (all P < 0.05). Conclusion The prevalence of osteoporosis in rural populations was higher than that in urban populations, and the factors associated with the risk of osteoporosis were similar in urban and rural populations.