To investigate this, we employed different models of β-cell stress: an acute β-cell toxicity model induced by treating mice with STZ (150 mg/kg), obesity mouse models displaying normoglycemia due to increased β-cell proliferation, function and pancreatic insulin content (i.e., dietary (HFD), and genetic (ob/ob mice on C57BL/6N background) [3, 22, 23], as well as diabetic models (db/db mice on BLKS background) exhibiting profound hyperglycemia, reduced plasma insulin levels due to β-cell dysfunction [24, 25] and apoptosis [26, 27]. This evidence concerns the gene INS and obesity disorder.