hepcidin

This is due to the release of hepcidin from the liver.

It was found that patients with β-thalassemia also have low hepcidin levels.

The overload of iron is associated with low levels of hepcidin.

It can increase iron absorption by suppressing the hormone hepcidin.

Twenty- and 22-amino acid metabolites of hepcidin also exist in the urine.

Carrying out studies in humans is difficult due to the lack of suitable hepcidin assay.

Taken together, these discoveries suggested that hepcidin regulates the release of iron in the body.

As a result, low hepcidin levels would result in increased intestinal iron absorption.

When body levels of iron are too low, then hepcidin in the duodenal epithelium is decreased.

Hepcidin levels in the liver are dramatically depressed in these knockout animals.

Hepcidin's antibacterial activity currently seems to be inconsistent.

Its primary mode of action is then through regulation of the iron storage hormone hepcidin.

Over the last few years, however, many investigators have come to feel that hepcidin is the central actor in producing anemia of chronic inflammation.

Ferroportin and hepcidin are critical proteins for the regulation of systemic iron homeostasis.

The structure of hepcidin has determined through solution NMR.

Infection leads to inflammation and the release of interleukin-6 (IL-6 ) which stimulates hepcidin expression.

Inflammation and erythropoietin, rather than the iron sensing pathway, are involved in the regulation of hepcidin expression.

Moreover cytokines stimulate hepcidin release from the liver, which is eventually responsible for the anemia of chronic disease.

In response to inflammatory cytokines, increasingly IL-6, the liver produces increased amounts of hepcidin.

Several mutations in hepcidin result in juvenile hemochromatosis.

The solution structure of hepcidin was determined at 325 K and 253 K in supercooled water.

Overexpression of hepcidin improves the outcome.

The liver produces hepcidin.

Bone morphogenetic protein signaling by hemojuvelin regulates hepcidin expression.

A small number of patients have mutations in the hepcidin (HAMP) gene.