Nutritional Modulation of Hepcidin in the Treatment of Various Anemic States

Abstract

Twenty years after its discovery, hepcidin is still considered the main regulator of iron homeostasis in humans. The increase in hepcidin expression drastically blocks the flow of iron, which can come from one’s diet, from iron stores, and from erythrophagocytosis. Many anemic conditions are caused by non-physiologic increases in hepcidin. The sequestration of iron in the intestine and in other tissues poses worrying premises in view of discoveries about the mechanisms of ferroptosis. The nutritional treatment of these anemic states cannot ignore the nutritional modulation of hepcidin, in addition to the bioavailability of iron. This work aims to describe and summarize the few findings about the role of hepcidin in anemic diseases and ferroptosis, as well as the modulation of hepcidin levels by diet and nutrients.

Dietary Artemisia arborescens Supplementation Effects on Growth, Oxidative Status, and Immunity of Gilthead Seabream (Sparus aurata L.)

“…In fish, hepcidin has been proven to participate in the immune response [65]. Moreover, in humans, some foods and nutrients have a known or potential ability to influence hepcidin release [67], but the relationship between dietary changes in fish and hepcidin is not currently studied [66]. Hepcidin gene expression was found to be down-regulated by increasing phytic acid (PA) levels in the head kidney, spleen, and skin of grass carp (Ctenopharyngodon idella).…”

Mechanisms of ferroptosis in nonalcoholic fatty liver disease and therapeutic effects of traditional Chinese medicine: a review

“…Hepcidin, a peptide produced and secreted by the liver, has a detrimental effect on the control of iron homeostasis ( 41 ). Iron can only be transported from cells to the blood during iron metabolism by membrane iron transporter protein 1 (FPN1).…”