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Mechanistically, combination treatment suppressed fatty acid synthesis, promoted mitochondrial function, and remodeled the gut microbiota

The primary defect is missense mutation in the HFE gene resulting in a cysteine to tyrosine substitution at aminoacidic 282 (C282Y), a protein that interacts with transferrin receptor 1 (TfR1) and regulates the expression of hepcidin, a key regulator of iron metabolism represented in Diagram B of Figure 2

Focusing on whole-food nutrition, lean proteins, vegetables, hydration, and meal preparation can help support better energy, digestion and appetite control

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