Models of glucose stimulated insulin secretion are commonly used to measure beta-cell function and to gain insight into the biological mechanisms of insulin release. Depending on the scope, the complexity of the model must be chosen appropriately. We present two models of minimal complexity, able to assess beta-cell function in an individual during intravenous and oral glucose perturbations and a comprehensive model of insulin secretion, describing intracellular events. We show how comparison of cellular and minimal models provides insight into the mechanisms underlying the different aspects of the minimal models, and yields biological meaning to their indices.