INS and Hyperglycemia: In beta cells, high-fat programming (i.e., maintenance on a diet of ≥40% mainly saturated fat as energy during critical developmental windows) induces beta cell hypoplasia and hypotrophy (altered beta cell structure) that diminishes beta cell function (altered beta cell physiology) evident by impaired glucose-stimulated insulin secretion (GSIS) resulting in insufficient insulin release that results in and exacerbates hyperglycemia, as demonstrated in neonatal, weanling, and adult progeny [1,2,3,4,5,6,7,8,9].