New molecular mechanisms of islet protection against diabetes

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Type 2 diabetes is an enormous health and economic burden. The mechanisms of β-cell compensation for insulin resistance and of β-cell failure in type 2 diabetes are unclear. This proposal will test the novel hypothesis that the adaptation of endoplasmic reticulum (ER) capacity mediates β-cell compensation, and that the failure of β-cell adaptation to ER stress causes diabetes. The studies will show that targeting ER capacity is an important novel strategy for type 2 diabetes therapy.