This experimental induction of increased insulin demand along with a reduction in functional β-cell mass is designed to mimic crucial manifestations in the pathogenesis of human type 2 diabetes, which can be accomplished within a condensed time frame (Kahn, 2001; Ferrannini et al., 2005; Weir and Bonner-Weir, 2013). Here, INS is linked to type 2 diabetes mellitus.