Talk:Hepcidin

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This review blames hepcidin for everything. JFW | T@lk 08:00, 8 December 2005 (UTC)

Needs to be more specific about timescales[edit]

Words like "Recently" and "soon after" are not as useful to the reader as actual dates. —Preceding unsigned comment added by 61.214.155.14 (talk) 08:31, 26 November 2007 (UTC)

Too much hepcidin, effects[edit]

When there's an excess of hepcidin (you have enough iron in your system) and an excess of iron passing the enterocytes in the intestine, how do enterocytes prevent too much iron entering their cytoplasma? — Preceding unsigned comment added by 80.218.105.42 (talk) 08:00, 4 June 2014 (UTC)

They don't. They just save it up and take it with them when they die and are shed.

69.179.29.83 (talk) 14:52, 1 July 2016 (UTC)

Restructuring[edit]

I know this straddles several areas but there is a fair amount of data on the gene and protein and less on the physiology from what I can tell so I think that the WP:MCBMOS style guide is must productive way to structure article.

My interest is from reading about erythropheresis in cancer but obviously iron homeostasis encompasses a lot more than that.

Jmwallach (talk) 01:44, 24 October 2014 (UTC)

Unclear or Erroneous[edit]

The sentence below is at best unclear. IMHO it should read "When the hepcidin level is abnormally low such as in hemochromatosis, iron overload occurs due to increased ferroportin mediated iron efflux from enterocytes".


When the hepcidin level is abnormally low such as in hemochromatosis, iron overload occurs due to decreased ferroportin mediated iron efflux.


69.179.29.83 (talk) 14:50, 1 July 2016 (UTC)