It is well known that the
iron content of the body is tightly regulated.
Iron excess induces adaptive changes that are differentially regulated in each tissue. The pancreas is particularly susceptible to
iron-related disorders. We studied the expression and regulation of key
iron proteins in the pancreas, duodenum and liver, using an animal model of
iron overload (female CF1 mice injected i.p. with
iron saccharate, colloidal
iron form). Divalent
metal transporter 1,
prohepcidin and
ferritin (pancreas, duodenum, liver) were assessed by immunohistochemistry; divalent
metal transporter 1 (pancreas, duodenum) by Western blot. In the
iron overloaded mice,
prohepcidin expression increased in islets of Langerhans and hepatocytes, and divalent
metal transporter 1 expression decreased in cells of islets and in enterocytes. In the
iron overloaded mice,
ferritin expression decreased in islets of Langerhans and increased in acinar cells;
hemosiderin was localized in connective tissue cells. The inverse relationship between divalent
metal transporter 1 and
prohepcidin may indicate a negative regulation by
hepcidin, and hence reduction of
iron stores in islets of Langerhans. Our data showed that in
iron overloaded mice model, induced by colloidal
iron form, a coordinated expression of key
iron proteins in the pancreas, duodenum and liver may occur. Further research will be necessary to determine the adaptive responses induced by
iron in the pancreas.