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Hepcidin And Regulation Of Iron Absorption And Homeostasis

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HEPCIDIN AND REGULATION OF IRON ABSORPTION AND HOMEOSTASIS

Abstract:
The micronutrient iron is crucial for life; however, maintenance of iron homoeostasis is critical since its deficiency or excess both leads to a pathological condition. Unlike like other nutrients, the iron homoeostasis is regulated at the level of absorption in the intestine and not via excretion. When the body iron store declines or when there is an increase in demand, the iron homoeostasis is maintained by the increase in absorption and vice versa. The recent biomedical advance has witnessed the hormone produced by liver, hepcidin as a prime regulator of iron homoeostasis by inhibiting iron absorption; however, the regulation of the hepcidin expression is complex and multifactorial. In this review, we explored and compared the recent advances in understanding the regulation of hepcidin expression.

Overview of iron homoeostasis
The micronutrient iron is vital for all living organism since it is required in the various metabolic process. The dietary requirement of iron for an average human is 1-2 milligram per day to compensate the minor loss of iron via bleeding, menstruation or the sloughing off of epithelial cells (Paul 2015) (figure 1). Despite its cruciality for life, iron is a double-edged sword and it is harmful in either extreme. When there is an excess iron in plasma, it binds to a low molecular weight molecule like citrate, acetate and albumin forming non-transferrin-bound iron (NTBI) which

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