Insulin degradation enzyme (IDE) knockout mice have elevated insulin levels, but exhibited impaired, rather than improved glucose homeostasis. A recent Nature publication identified a physiologically active IDE inhibitor from a DNA-templated macrocycle library, allowing the study of IDE in a more specific manner than the knockout mice could. Treatment of both lean and obese mice with this inhibitor showed that IDE regulated not only insulin but also glucagon and amylin, demonstrating the feasibility of modulating IDE activity as a new strategy to treat type-2 diabetes. What are the underlying mechanisms?




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