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In individuals with congenital hyperinsulinism due to inactivating mutations in the genes encoding the beta cell K ATP channels, the GLP-1 receptor antagonist, exendin-(9-39), increases fasting plasma glucose and prevents protein-induced hypoglycemia

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These adverse effects not only increase the risk of long-term organ damage and treatment failure but also contribute to higher mortality rates and reduced quality of life, even during remission phases (Basta et al., 2020)

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