No abstract available.
Cardio-Renal Syndrome ; Hepcidins

No abstract available.
Anemia* ; Arthritis, Rheumatoid* ; Hepcidins* ; Humans

Hematologic Diseases ; drug therapy ; Hepcidins ; therapeutic use ; Homeostasis ; Humans ; Iron

OBJECTIVE: To explore the possible etiological factors of iron overload through detecting plasma hepcidin level of adult males at Tibet plateau. METHODS: 81 Tibetan male adult patients hospitalized in our department during January 2017 - December 2018 were selected, and divided into iron overload group and non-iron overload group. The difference in serum ferritin, serum iron, total iron binding capacity, hemoglobin, HBSAg, ALT, AST, albumin, creatinine and hepcidin of patients in each group were tested. To analyze the differences between groups. The regression analysis was applied to analyze the relationship between laboratory index and hepcidin. RESULTS: The plasma hepcidin of iron overload group was significantly higher than that of the non-iron overload group [93.69 (65.57-133.92) ng/ml vs 63.93 (40.01-90.65) ng/ml] (P=0.005). And there was a positive correlation between plasma hepcidin and ferritin (β=0.03 ng/ml，95%CI 0.01-0.05) (P<0.01) and BMI (β=5.71 ng/ml，95%CI 0.54-10.88) (P<0.05）. CONCLUSION Iron overload at Tibet plateau can not be attributed to hepcidin deficiency in Tibetan adult male patients. Iron metabolism disorders in Tibetan population may be associated with metabolic syndrome.
Adult ; Ferritins ; Hepcidins ; Humans ; Iron ; Iron Overload ; Male ; Tibet

Hepcidin is a small cystein-rich cationic peptide produced mainly by the liver. It was initially isolated from human plasma and exhibited antimicrobial activity. Recently, several lines of evidence have suggested that hepcidin is a key regulator of iron metabolism at the whole body level and is relative to inflammation, infection, hypoxia and anemia. Hepcidin, is implicated in duodenal iron absorption and iron mobilization from reticuloendothelial macrophages. The major mechanism of hepcidin function seems to be the regulation of transmembrane iron transport. As both iron deficiency and iron excess are associated with cellular dysfunction, so hepcidin or hepcidin-related therapeutics could find a place in the treatment of various diseases such as hemochromatosis and anemia of chronic disease. To elucidate biological function of hepcidin further and use it for other research, it is necessary to produce enough hepcidin through DNA recombinant technique. As a highly successful system for the production of a variety of heterologous proteins, the methylotrophic Pichia pastoris system has the probability for a high level production of hepcidin. The subject of this paper is to summarize the regulation of hepcidin gene expression and the understanding of functions of hepcidin. At last, giving a prospect of production hepcidin by gene engineer.
Antimicrobial Cationic Peptides ; biosynthesis ; genetics ; physiology ; Hepcidins ; Humans ; Iron ; metabolism ; Protein Engineering ; methods

BACKGROUND: Hepcidin, a key regulator of iron homeostasis, is associated with iron metabolism imbalance in patients with chronic kidney disease (CKD). However, serum hepcidin level in anemic patients with CKD presents a contradictory picture. We investigated the relationship between serum hepcidin-25 level and iron parameters in patients with CKD. METHODS: We defined and categorized patients with CKD according to the Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines. We analyzed the relationship between serum hepcidin-25 level and iron parameters [serum iron, total iron-binding capacity (TIBC), unbound iron-binding capacity (UIBC), transferrin saturation, and ferritin levels] according to the CKD stage and clinical and laboratory characteristics. RESULTS: Hb level, TIBC, and UIBC decreased and ferritin level increased (Ptrend<0.001) (stage 1-2, 28; stage 3, 40; stage 4, 36; stage 5, 42) as the CKD stage progressed. Serum hepcidin-25 level showed no significant trend with the progressing CKD stage [stage 1-2, 13.7 (3.7-25.0) ng/mL; stage 3, 14.0 (0.8-26.5) ng/mL; stage 4, 13.9 (2.0-32.1) ng/mL; stage 5, 13.8 (0.5-42.4) ng/mL; Ptrend=0.618]. No significant relationship was noted between serum hepcidin-25 level and kidney function parameters, Hb levels, or iron parameters (P>0.05). CONCLUSIONS: Serum hepcidin-25 level was not found to be associated with iron parameters or clinical status of CKD patients in our study. Determination of hepcidin-25 levels may not provide more information than conventional iron parameters in monitoring iron metabolism in CKD patients. However, further studies are needed to establish the clinical utility of hepcidin measurement in CKD patients.
Anemia ; Ferritins ; Hepcidins* ; Homeostasis ; Humans ; Iron* ; Kidney ; Kidney Diseases ; Metabolism ; Renal Insufficiency, Chronic* ; Transferrin

OBJECTIVETo investigate the multiple iron metabolism-related genes expression, its regulation by iron and the expression correlation among the genes in rat tissues.

METHODSTwo groups (n=30) of Sprague-Dawley female weanling rats were fed with a control diet and an iron deficient diet respectively for 4 weeks. All rats were then sacrificed, and blood and tissue samples were collected. The routine blood examination was performed with a veterinary automatic blood cell analyzer. Elemental iron levels in liver, spleen and serum were determined by atomic absorption spectrophotometry. The mRNA expression of genes was detected by real-time fluorescence quantitative PCR.

RESULTSAfter 4 weeks, the hemoglobin (Hb) level and red blood cell (RBC) count were significantly lower in the iron deficient group compared with those in the control group. The iron levels in liver, spleen and serum in the iron deficient group were significantly lower than those in the control group. In reference to small intestine, the relative expression of each iron-related gene varied in the different tissues. Under the iron deficiency, the expression of these genes changed in a tissue-specific manner. The expression of most of the genes significantly correlated in intestine, spleen and lung, but few correlated in liver, heart and kidney.

CONCLUSIONFindings from our study provides new understandings about the relative expression, regulation by iron and correlation among the mRNA expressions of transferrin receptors 1 and 2, divalent metal transporter 1, ferritin, iron regulation proteins 1 and 2, hereditary hemochromatosis protein, hepcidin, ferroportin 1 and hephaestin in intestine, liver, spleen, kidney, heart, and lung of rat.

Animals ; Ferritins ; blood ; Gene Expression ; Hepcidins ; Iron ; Liver ; metabolism ; Rats ; Rats, Sprague-Dawley

Hepcidin can regulate cell irons' efflux transport. The expression of hepcidin can be influenced by the body signals (such as serum ferritin and erythropoietin levels) as well as inflammation, hypoxia and other disease states. These stimulus activate the signaling pathway of BMP-the SMAD, the JAK-STAT and HIF1 through the liver parenchymal cell surface type I transmembrane glycoprotein of HFE, transferrin receptor 1, 2, hepcidin regulatory proteins, thereby changing the hepcidin gene transcription, regulating the expression levels of hepcidin. However, the molecular mechanism that regulate hepcidin expression is unclear. From the signal factors that affect hepcidin expression and signaling pathways involved in its expression, the latest research progress on regulatory mechanism of hepcidin are summarized.
Animals ; Antimicrobial Cationic Peptides ; metabolism ; Hepcidins ; Humans ; Membrane Proteins ; metabolism ; Signal Transduction

Antimicrobial Cationic Peptides ; biosynthesis ; Hepacivirus ; pathogenicity ; Hepcidins ; Iron ; metabolism ; Liver ; chemistry ; metabolism ; pathology

Anemia of chronic disease is normocytic and normochromic. One of the mechanisms is misbalance of iron metabolism. Hepcidin, a kind of protein secreted by liver is considered to be the hormone regulating iron metabolism. It binds to ferroportin and induces the latter one's internalization. Thus, iron transportation from iron storage cells to serum is reduced. Cytokines are elevated in chronic disease. They stimulate hepcidin expression in liver through JAK2/STAT3 pathway. As a result, iron absorption and reabsorption is blocked, which leads to the misbalance of iron metabolism in anemia of chronic disease. In this article, the hepcidin and its relation to iron metabolism and anemia in chronic disease are reviewed.
Anemia ; metabolism ; Antimicrobial Cationic Peptides ; metabolism ; Chronic Disease ; Hepcidins ; Humans ; Iron ; metabolism