IRS1 and metabolic syndrome: Whereas physiological iron bioavailability is indispensable for hemoglobin synthesis and metalloenzyme catalysis, disrupted iron homeostasis manifesting as hepatic iron overload has been mechanistically linked to mitochondrial oxidative damage, insulin receptor substrate-1 (IRS-1) serine phosphorylation, and NF-κB-mediated chronic low-grade inflammation—three cardinal pathomechanisms driving MetS progression [9,10].