This mouse study fed a carbonyl-iron-enriched diet for two weeks and tracked untargeted blood, plasma and liver metabolites by liquid chromatography with high-resolution mass spectrometry. Iron loading raised circulating glucose, aspartic acid and hydroxybutyric acids, lowered lactate and malate, stimulated the liver urea cycle and increased markers of oxidative stress alongside higher liver glutathione. The authors read this as a reprogramming of glucose handling and the Krebs cycle.
Key numbers
- Diets: standard chow with 180 mg iron per kg (n = 3) versus chow supplemented with 25 g carbonyl iron per kg (n = 5), for 14 days (Section 2.2, p. 3).
- Sampling at days 0, 7 and 14 by volumetric absorptive microsampling; liver and plasma at day 14 (Methods, p. 3).
- The authors state that the iron diet increased plasma iron and liver ferritin expression (Figure S2, not reproduced in the main text).
Methods (brief)
Male wild-type mice were randomized to diets. Blood microsamples, heparin plasma and unperfused liver were extracted and profiled by untargeted LC-high-resolution MS, with principal component analysis and t-tests or two-way ANOVA for change over time.
Evidence fitness
Supports animal evidence that a large dietary iron load perturbs energy metabolism and redox balance within two weeks. The authors note the diet iron is supra-physiological; the study cannot be scaled to human dietary exposure.
Limitations
Very small groups (3 and 5), male mice only, unperfused liver, a single high dose and short duration. Iron status measurements are only in supplementary material.
Related evidence
Update history
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