Indeed, the possible mechanisms of CVD in Abnl-GT-IR may relate to insulin resistance-induced hyperinsulinemia-linked sodium retention, and increased sympathetic activation (low NT-proBNP, associating with lower eGFR), oxidative stress leading to cellular injury and apoptosis (association with hs-cTnT), which may result in decreased cardiac contractility, production of advanced glycation end-products contributing to cardiac fibrosis and inflammation (high fibrinogen and hsCRP)7,52. This evidence concerns the gene NPPB and hyperinsulinism.