Using a human model of partial pancreatectomy, we recently demonstrated that beta cell function and patterns of insulin secretion differed significantly among non-diabetic individuals, and that only pre-existing impairments in beta cell function, i.e. reduced first-phase insulin release (model-derived reduced glucose sensitivity and rate sensitivity) and defective proinsulin processing in the granules, predicted impairment in glucose tolerance and diabetes [5–7]. Here, INS is linked to diabetes mellitus.