Iron-regulatory hormone that acts as an erythroid regulator after hemorrhage: produced by erythroblasts following blood loss and mediates suppression of hepcidin (HAMP) expression in the liver, thereby promoting increased iron absorption and mobilization from stores (PubMed:24880340). Promotes lipid uptake into adipocytes and hepatocytes via transcriptional up-regulation of genes involved in fatty acid uptake (PubMed:22351773). Homodimer; disulfide-linked. May form heteromeric complexes with C1QTNF2 and C1QTNF12 and, to a lesser extent, with C1QTNF5 and C1QTNF10. Predominantly expressed in skeletal muscle and, at much lower levels, in other tissues, including lung, eye, smooth muscle, heart, brain and kidney. Within skeletal muscles, higher expression levels in soleus as compared with plantaris. Found in blood (at protein level). Following EPO treatment, only expressed in bone marrow and spleen (PubMed:24880340). Females tend to have higher circulating levels than males. Obese mice tend to have lower expression and circulating levels as compared to lean animals. In the myoblast C2C12 cell line, expression is increased upon differentiation into myotubes. Up-regulated by intracellular increase in cAMP levels, such as those elicited by forskolin and epinephrine treatments, and increase in calcium (ionomycine). Up-regulated by exercise in skeletal muscle (at the mRNA level) and blood (at protein level). Drastically down-regulated by fasting. Up-regulated in skeletal muscle by refeeding; the extent of induction by refeeding may be dependent upon the muscle fiber type, being much higher in soleus than in plantaris. Both glucose and lipid are equally potent in this induction, in the absence of any gut-derived hormones. Highly induced within 4 hours of bleeding (PubMed:24880340). N-glycosylated. Mice are viable and fertile without any abnormal phenotypic features in normal conditions but show transient hemoglobin deficit after hemorrhage and exhibit a delay in recovery from blood loss. They also fail to suppress hepcidin rapidly. Mice with thalassemia intermedia show high levels of Erfe expression, contributing to the suppression of hepcidin and the systemic iron overload characteristic of thalassemia. Belongs to the adipolin/erythroferrone family.