Anemia occurs with undernutrition, yet even though there is reduced hemoglobin and serum iron concentrations in these states, tissue iron stores remain intact or may increase.  Both short term starvation and severe food deprivation contribute to reduced iron absorption leading to reduced iron available for erythropoiesis.  Hepcidin may mediate these effects but it is not known whether hepcidin and iron homeostasis are similarly impacted during mild or moderate food deprivation.  Murphy and colleagues conducted a study to address this void in our knowledge and published their results in the October 2022 issue of The Journal of Nutrition.

Mice were provided ad libitum access to diet, or exposed to differing levels of food deprivation (10, 20, 40, 60, 80 or 100% of ad libitum).  Samples to determine hepcidin and iron status were collected at termination, which occurred at 48h, 1 week, 2 weeks or 3 weeks, depending on the extent of food deprivation.

Expression of liver hepcidin was positively correlated with the extent of food deprivation at all time points.  Serum hepcidin was elevated with 10 and 20% food deprivation at 3 weeks, as was liver hepcidin expression.  Serum iron was reduced and liver nonheme iron increased by 10 and 20% food deprivation at 3 weeks.  There was a positive correlation among liver gluconeogenic enzymes and liver Bmp6 with liver hepcidin expression, but not markers of inflammation at 3 weeks.  The authors concluded that food deprivation causes hypoferremia and tissue iron sequestration, and that changes in hepcidin may be responsible for the disturbances in iron homeostasis.


Robert D Murphy, Kelsey M James, James R Ippolito, David E Barney, Jr, Katelyn M Miller, Nancy E Murphy, Jess A Gwin, Stefan M Pasiakos, James P McClung, Lee M Margolis, Stephen R Hennigar, Mild to Moderate Food Deprivation Increases Hepcidin and Results in Hypoferremia and Tissue Iron Sequestration in Mice, The Journal of Nutrition, Volume 152, Issue 10, October 2022, Pages 2198–2208,

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