Abstract EN:

The laboratory which welcomed me in thesis identified the regulator of the iron homeostasis, hepcidin. The production of hepcidin is modulated according to the iron demands of the body : in the presence of iron, the synthesis of hepcidin is increased to avoid the excess of the metal which is toxic, and, on the contrary, hepcidin is decreased to allow an effective mobilization of the metal. I participated in the characterization of the phenotype of mouse KO HEPC1 which present a multivisceral iron overload with a particularly important hepatic and pancreatic accumulation of iron. In this murin model, I tried to establish the link between the iron metabolism and the glucose metabolism. I studied the mechanisms of physiopathological regulation of the hepcidin by the iron in a system of primary culture of hepatocytes. This system of culture of hepatocytes allowed me to study ferroportin, the iron excarrier and the mechanisms of mobilization of the iron of the hepatocyte.