June 14, 2024Diabetes

286-OR: JNK3—A Key Downstream Target of Incretin Responses in ß-Cells

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Impaired insulin secretion and glucose intolerance occur following oral challenge in mice lacking beta-cell JNK3, which links this kinase directly to incretin responses.
Assessment of incretin responses in knockout mice and human islets showed reduced GLP1R expression, with marked decreases in CREB phosphorylation and downstream IRS2.
Supports JNK3 as a promising therapeutic target for incretin-based diabetes therapy to protect beta-cells—mouse model and human islet study; further preclinical work needed.

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Implication

Preclinical study reveals impaired incretin-induced insulin secretion and reduced GLP1R in beta-cell JNK3-knockout mice, highlighting JNK3 as a potential therapeutic target.

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NETO et al. (2024) studied this question.

synapsesocial.com/papers/68e64c51b6db6435875dd5c7 https://doi.org/10.2337/db24-286-or

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Implication

Preclinical study reveals impaired incretin-induced insulin secretion and reduced GLP1R in beta-cell JNK3-knockout mice, highlighting JNK3 as a potential therapeutic target.

286-OR: JNK3—A Key Downstream Target of Incretin Responses in ß-Cells

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Implication

Cite This Study

286-OR: JNK3—A Key Downstream Target of Incretin Responses in ß-Cells

Key Points

Discussion

Implication

Cite This Study

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