Hepcidin Level Changes in Type 2 Diabetes

Abstract

Background: Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion or insulin action, or both. Diabetes and its complications have become a major public health problem in the world and its prevention has become a public health priority. Hepcidin, a 25-amino-acid antimicrobial peptide, is the central regulator of iron homeostasis. Under normal circumstances, hepcidin expression and subsequent release into plasma prevents further absorption of iron from the duodenal enterocytes by preventing the efflux of iron by ferroportin channels, hence reduced amounts of iron delivery via transferrin to hepatocytes. In response to iron loading, hepcidin expression increased to prevent the further uptake of iron. Conversely, during iron deficiency, hepcidin expression decreased.