A 59-year-old Japanese woman presented with hyperferritinemia. We decided against iron removal treatment because there were no symptoms or signs of iron-induced organ damage. A follow-up study revealed a gradual increase in transferrin saturation. The patient underwent a second examination at 66 years old. A liver biopsy showed substantial iron deposits in hepatocytes and Kupffer cells but no inflammation or fibrosis. Serum hepcidin-25 levels were highly parallel with hyperferritinemia. A genetic analysis revealed a G80S mutation in SLC40A1. These features are compatible with those of ferroportin disease. The patient remained asymptomatic at 70 years old, suggesting that the iron-loading condition may have been benign.
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http://dx.doi.org/10.2169/internalmedicine.2392-23 | DOI Listing |
Arq Gastroenterol
January 2025
Universidade Estadual de Campinas, Programa de Pós-Graduação em Farmacologia, Campinas, SP, Brasil.
Background: Hepcidin's main function is to control iron availability to hematopoiesis. However, it has been shown that hepcidin may have an additional role in intestinal inflammation, as intestinal cells and leukocytes increase the production in experimental colitis and Crohn's disease.
Objective: Using an HT-29 cell as a model, we investigated the role of hepcidin in intestinal inflammation.
Fish Shellfish Immunol
January 2025
Guangdong Provincial Water Environment and Aquatic Products Security Engineering Technology Research Center, Guangzhou Key Laboratory of Aquatic Animal Diseases and Waterfowl Breeding, College of Animal Sciences and Technology, Zhongkai University of Agriculture and Engineering, Guangzhou, Guangdong Province, 510222, China. Electronic address:
Intravascular hemolysis releases hemoglobin (Hb) from red blood cells under specific conditions, yet the effect of hemolysis in aquaculture systems remain poorly understood. In this study, a continuous hemolysis model for grass carp was established by injection of phenylhydrazine (PHZ) to investigate the mechanistic impacts of sustained hemolysis. PHZ-induced hemolysis altered liver color, and subsequent hematoxylin and eosin staining revealed substantial Hb accumulation in the head kidney, accompanied by inflammatory cell infiltration and vacuolization in liver tissue.
View Article and Find Full Text PDFCurr Obes Rep
January 2025
Department of Endocrinology and Metabolism, Zhuhai People's Hospital (The Affiliated Hospital of Beijing Institute of Technology, Zhuhai Clinical Medical College of Jinan University), Zhuhai, China.
Purpose Of Review: Review the latest data regarding the intersection of adipose tissue (AT) and iron to meet the needs of AT metabolism and the progression of related diseases.
Recent Findings: Iron is involved in fundamental biological metabolic processes and is precisely fine-tuned within the body to maintain cellular, tissue and even systemic iron homeostasis. AT not only serves as an energy storage depot but also represents the largest endocrine organ in the human body, maintaining systemic metabolic homeostasis.
Hepatol Commun
January 2025
Liver Research Center, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health and National Clinical Research Center of Digestive Diseases, Beijing, China.
Background: Hepcidin, a peptide hormone primarily produced by the liver, regulates iron metabolism by interacting with its receptor, ferroportin. Studies have demonstrated that hepcidin participates in the progression of liver fibrosis by regulating HSC activation, but its regulatory effect on hepatocytes remains largely unknown.
Methods: A carbon tetrachloride (CCl4)-induced liver fibrosis model was established in C57BL/6 wild-type (WT) and hepcidin knockout (Hamp-/-) mice.
Elevated circulating hepcidin levels have been reported in patients with pulmonary artery hypertension (PAH). Hepcidin has been shown to promote proliferation of human pulmonary artery smooth muscle cells (PASMCs) in vitro, suggesting a potential role in PAH pathogenesis. However, the role of human pulmonary artery endothelial cells (PAECs) as either a source of hepcidin, or the effect of hepcidin on PAEC function is not as well described.
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