To examine the temporal changes of islet Mt1 and Mt2 gene expression under the states of beta-cell compensation and failure, we used two mouse models of obesity with an opposite propensity for the development of diabetes: (1) the diabetes resistant ob/ob mice on the C57BL/6J genetic background and (2) the diabetes-prone db/db mice on the C57BL/KsJ genetic background, which exhibit a progressive age-dependent beta-cell decompensation and development of hyperglycemia [112,113,114]. Here, MT1H is linked to obesity due to melanocortin 4 receptor deficiency.