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Genetic variants that modulate iron homeostasis and tissue levels of iron are the main determinants of serum levels of ferritin in individuals with metabolic dysfunction, raising the hypothesis that iron accumulation might be implicated in the pathogenesis of insulin resistance and the related organ damage

Currently, whether there is functional redundancy in the regulation of the same immune pathway (e.g., NF-B) by different metabolites (e.g., SCFAs, polysaccharides), as well as their synergistic or antagonistic relationships, remains unclear

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