The molecular events causing increased insulin resistance and secretion and early β-cell failure in diabetes are not well understood. Gema Medina-Gomez and colleagues define a mouse model, derived from insulin-resistant ob/ob mice, that lacks the nuclear receptor PPARγ2. Lipid profiles and other changes associated with early phase diabetes are evident in animals only 4 weeks old. β cells in the pancreas are initially protected from damage, showing increased insulin production and cell expansion. Thus, these mice demonstrate changes similar to humans in the early stage of diabetes.

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