scholarly journals MyD88 Adaptor Protein Is Required for Appropriate Hepcidin Induction in Response to Dietary Iron Overload in Mice

2018 ◽  
Vol 9 ◽  
Author(s):  
Antonio Layoun ◽  
Macha Samba-Mondonga ◽  
Gabriela Fragoso ◽  
Annie Calvé ◽  
Manuela M. Santos
PLoS ONE ◽  
2009 ◽  
Vol 4 (9) ◽  
pp. e7212 ◽  
Author(s):  
Alejandra Rodriguez ◽  
Tiina Luukkaala ◽  
Robert E. Fleming ◽  
Robert S. Britton ◽  
Bruce R. Bacon ◽  
...  

Hepatology ◽  
1990 ◽  
Vol 11 (5) ◽  
pp. 798-804 ◽  
Author(s):  
Antonello Pietrangelo ◽  
Emilio Rocchi ◽  
Luisa Schiaffonati ◽  
Ezio Ventura ◽  
Gaetano Cairo

Author(s):  
Manfred Nairz ◽  
Andrea Schroll ◽  
David Haschka ◽  
Stefanie Dichtl ◽  
Piotr Tymoszuk ◽  
...  

1990 ◽  
Vol 39 (1) ◽  
pp. 123-128 ◽  
Author(s):  
A. Pietrangelo ◽  
R. Grandi ◽  
A. Tripodi ◽  
A. Tomasi ◽  
D. Ceccarelli ◽  
...  

Toxicon ◽  
2013 ◽  
Vol 67 ◽  
pp. 37-46 ◽  
Author(s):  
Vanessa Moreira ◽  
Catarina Teixeira ◽  
Henrique Borges da Silva ◽  
Maria Regina D'Império Lima ◽  
Maria Cristina Dos-Santos

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1400 ◽  
Author(s):  
Machi Atarashi ◽  
Takeshi Izawa ◽  
Mutsuki Mori ◽  
Yohei Inai ◽  
Mitsuru Kuwamura ◽  
...  

Chronic liver disease is an intractable disease, which can progress to cirrhosis and hepatocellular carcinoma. Hepatic iron overload is considered to be involved in the progression of chronic liver diseases; however, the mechanism remains to be elucidated. Here we investigate the role of dietary iron overload using chemically-induced liver cirrhosis model. Rats were fed a high-iron or standard diet and were injected intraperitoneally with thioacetamide (TAA) or saline twice a week for 20 weeks. Rats with TAA treatment (TAA group) had progressive liver cirrhosis characterized by persistent hepatocellular injury, mononuclear cell inflammation and bridging fibrosis; these lesions were markedly reduced in rats with iron feeding and TAA treatment (Fe-TAA group). Rats with iron feeding alone (Fe group) had no evidence of liver injury. Hepatic expression of cleaved caspase-3, but not phospho-RIP3, was decreased in Fe-TAA group compared with that in TAA group. The number of TUNEL-positive (terminal deoxynucleotidyl transferase dUTP nick end labeling) apoptotic hepatocytes was lower in the Fe-TAA group than in the TAA group. Hepatic xenobiotic metabolism and lipid peroxidation were shown to be less related to the abrogation of liver cirrhosis. Our results suggested that dietary hepatic iron overload abrogates chemically-induced liver cirrhosis in rats, which could partly involve decreased hepatocellular apoptosis.


2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Francesca La Carpia ◽  
Boguslaw S. Wojczyk ◽  
Medini K. Annavajhala ◽  
Abdelhadi Rebbaa ◽  
Rachel Culp-Hill ◽  
...  

Abstract Iron is essential for both microorganisms and their hosts. Although effects of dietary iron on gut microbiota have been described, the effect of systemic iron administration has yet to be explored. Here, we show that dietary iron, intravenous iron administration, and chronic transfusion in mice increase the availability of iron in the gut. These iron interventions have consistent and reproducible effects on the murine gut microbiota; specifically, relative abundance of the Parabacteroides and Lactobacillus genera negatively correlate with increased iron stores, whereas members of the Clostridia class positively correlate with iron stores regardless of the route of iron administration. Iron levels also affected microbial metabolites, in general, and indoles, in particular, circulating in host plasma and in stool pellets. Taken together, these results suggest that by shifting the balance of the microbiota, clinical interventions that affect iron status have the potential to alter biologically relevant microbial metabolites in the host.


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