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Glycemia shifts pancreatic islet rhythmicity by influencing interactions between δ cells and α cells (opens in new tab)

Glycemic fluctuations trigger a fast-slow oscillation switch in islet Ca2+ activity in vivo. We show that this rhythmicity depends on α-δ cell interactions, is impaired in diabetes, and is restored by GLP1R signaling. Our findings highlight a paracrine-driven coordination of islet dynamics supporting blood glucose stability.

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