Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

A high-fat diet modulates iron metabolism but does not promote liver fibrosis in hemochromatotic Hjv⁻/⁻ mice.

American journal of physiology. Gastrointestinal and liver physiology - 15 Feb 2015

Padda Ranjit Singh, Gkouvatsos Konstantinos, Guido Maria, Mui Jeannie, Vali Hojatollah, Pantopoulos Kostas

Abstract excerpt

Hemojuvelin (Hjv) is a membrane protein that controls body iron metabolism by enhancing signaling to hepcidin. Hjv mutations cause juvenile hemochromatosis, a disease of systemic iron overload. Excessive iron accumulation in the liver progressively leads to inflammation and disease, such as fibrosis, cirrhosis, or hepatocellular cancer. Fatty liver (steatosis) may also progress to inflammation (steatohepatitis)...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Diet, High-Fat
Share to Fatty Liver

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to GPI-Linked Proteins

Share to Hemochromatosis

Share to Hemochromatosis Protein

Share to Hepcidins

Share to Liver Cirrhosis

Share to Weight Gain

Source

Identifiers

PMID: 25501544
DOI: 10.1152/ajpgi.00137.2014

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A high-fat diet modulates iron metabolism but does not promote liver fibrosis in hemochromatotic Hjv⁻/⁻ mice.PMID 25501544Read ↗

Hemojuvelin is essential for dietary iron sensing, and its mutation leads to severe iron overloadSemantic proximity Read ↗

Mouse models of hereditary hemochromatosis do not develop early liver fibrosis in response to a high fat dietSemantic proximity Read ↗

Iron-dependent regulation of hepcidin in Hjv-/- mice: evidence that hemojuvelin is dispensable for sensing body iron levels.Semantic proximity Read ↗

Targeted disruption of hepcidin in the liver recapitulates the hemochromatotic phenotype.Semantic proximity Read ↗

Disruption of hemochromatosis protein and transferrin receptor 2 causes iron-induced liver injury in mice.Semantic proximity Read ↗

Hepatic HIF2α modulates extra-hepatic disease-associated phenotypes during metabolic dysfunction-associated steatotic liver diseaseSemantic proximity Read ↗

The effect of the metabolic syndrome, hepatic steatosis and steatohepatitis on liver fibrosis in hereditary hemochromatosis.Semantic proximity Read ↗

Gnpat does not play an essential role in systemic iron homeostasis in murine model.Semantic proximity Read ↗

Evaluation of high-fat high-fructose diet treatment in factor VIII (coagulation factor)-deficient mouse model.Semantic proximity Read ↗

Bone phenotyping of murine hemochromatosis models with deficiencies of Hjv, Alk2, or Alk3: The influence of sex and the bone compartment.Semantic proximity Read ↗

Hepcidin expression does not rescue the iron-poor phenotype of Kupffer cells in Hfe-null mice after liver transplantation.Semantic proximity Read ↗

Defective targeting of hemojuvelin to plasma membrane is a common pathogenetic mechanism in juvenile hemochromatosisSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.