LGALS3 and Hyperglycemia: The persistent elevation of GDF15, sST2, and Galectin-3 despite marked HbA1c reduction may reflect ongoing adipose tissue inflammation independent of hyperglycemia [34], which could be mediated by different mechanisms, such as oxidative stress, lipotoxicity [28], or epigenetically mediated changes in adipocyte and myocardial gene expression [31].