Vitamin A deficiency modulates iron metabolism via ineffective erythropoiesis

Cunha, Marcela de Sá Barreto da; Siqueira, Egle M. A.; Trindade, Luciano S.; Arruda, Sandra Fernandes

doi:10.1016/j.jnutbio.2014.05.005

Cited by 34 publications

(28 citation statements)

References 52 publications

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“…For convenience, we will refer to Hamp mRNA, but hepcidin ( Hepc ) expression. Dietary VA impacts serum iron homeostasis through hepcidin (da Cunha et al, 2014). Hepc is expressed exclusively in hepatocytes and regulates iron homeostasis by inhibition of ferroportin, an iron transport channel, to prevent gut absorption and macrophage recycling of erythrocytes (Ganz, 2013).…”

Section: Resultsmentioning

confidence: 99%

Cyp1b1 deletion and retinol deficiency coordinately suppress mouse liver lipogenic genes and hepcidin expression during post-natal development

Maguire

Larsen

Foong

et al. 2017

Molecular and Cellular Endocrinology

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Cyp1b1 deletion and gestational vitamin A deficiency (GVAD) redirect adult liver gene expression. A matched sufficient pre- and post-natal diet, which has high carbohydrate and normal iron content (LF12), increased inflammatory gene expression markers in adult livers that were suppressed by GVAD and Cyp1b1 deletion. At birth on the LF12 diet, Cyp1b1 deletion and GVAD each suppress liver expression of the iron suppressor, hepcidin (Hepc), while increasing stellate cell activation markers and suppressing post-natal increases in lipogenesis. Hepc was less suppressed in Cyp1b1−/− pups with a standard breeder diet, but was restored by iron supplementation of the LF12 diet. Conclusions The LF12 diet delivered low post-natal iron and attenuated Hepc. Hepc decreases in Cyp1b1−/− and GVAD mice resulted in stellate activation and lipogenesis suppression. Endothelial BMP6, a Hepc stimulant, is a potential coordinator and Cyp1b1 target. These neonatal changes in Cyp1b1−/− mice link to diminished adult obesity and liver inflammation.

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Section: Resultsmentioning

confidence: 99%

Cyp1b1 deletion and retinol deficiency coordinately suppress mouse liver lipogenic genes and hepcidin expression during post-natal development

Maguire

Larsen

Foong

et al. 2017

Molecular and Cellular Endocrinology

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“…In other studies investigating vitamin A and its relationship with iron metabolism in Mus musculus rats treated with retinol palmitate (4,000 IU/kg) for 22 days, the treatment increased the mRNA levels of hepcidin and ferritin, favouring the accumulation of iron in the liver, as well as increased oxidative and inflammatory stress [77,78,79]. …”

Section: Hepcidinmentioning

confidence: 99%

Hepcidin: Homeostasis and Diseases Related to Iron Metabolism

et al. 2017

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Iron is an essential metal for cell survival that is regulated by the peptide hormone hepcidin. However, its influence on certain diseases is directly related to iron metabolism or secondary to underlying diseases. Genetic alterations influence the serum hepcidin concentration, which can lead to an iron overload in tissues, as observed in haemochromatosis, in which serum hepcidin or defective hepcidin synthesis is observed. Another genetic imbalance of iron is iron-refractory anaemia, in which serum concentrations of hepcidin are increased, precluding the flow and efflux of extra- and intracellular iron. During the pathogenesis of certain diseases, the resulting oxidative stress, as well as the increase in inflammatory cytokines, influences the transcription of the HAMP gene to generate a secondary anaemia due to the increase in the serum concentration of hepcidin. To date, there is no available drug to inhibit or enhance hepcidin transcription, mostly due to the cytotoxicity described in the in vitro models. The proposed therapeutic targets are still in the early stages of clinical trials. Some candidates are promising, such as heparin derivatives and minihepcidins. This review describes the main pathways of systemic and genetic regulation of hepcidin, as well as its influence on the disorders related to iron metabolism.

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“…Furthermore, atRA is thought to play a part in controlling iron metabolism, another essential nutrient for Mtb survival [49,50]. Our group has demonstrated the effect of alveolar macrophage derived atRA on the stimulation of regulatory T Cells (Tregs) in the lungs through the transcription factor FoxP3 in conjunction with TGF-β1, leading to downregulation of the pro-inflammatory effects of the innate immune system and upregulation of anti-inflammatory proteins -namely interleukin-10 (IL-10) [51].…”

Section: Vitamin Amentioning

confidence: 99%