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This study aims to explore the role of JNK3 in β-cell incretin responsiveness and metabolic regulation.

c‐Jun N‐terminal kinase 3 as a permissive regulator of β‐cell incretin responsiveness

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This study aims to explore the role of JNK3 in β-cell incretin responsiveness and metabolic regulation.
Used β-cell-specific JNK3 knockout mice
Conducted experiments in human islets
Evaluated glucose tolerance and insulin secretion responses
Loss of JNK3 impairs glucose tolerance and insulin secretion during nutrient challenges
JNK3 loss reduces GLP-1 receptor expression
Inhibition of JNK3 attenuates protective effects of GLP-1 receptor activation

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Findings demonstrate JNK3 maintains incretin responsiveness in β-cells, suggesting impacts on insulin secretion and glucose metabolism.

Y. Yamazaki (2026) studied this question.

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