#3604. Carbon monoxide enhances calcium transients and glucose-stimulated insulin secretion from pancreatic ?-cells by activating Phospholipase C signal pathway in diabetic mice

October 2026publication date
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Medicine
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Abstract:
Insulin secretion from pancreatic cells is increased to deal with the elevated blood glucose. Previous studies have reported that islet-produced carbon monoxide (CO) is associated with increased glucose-stimulated insulin secretion from cells. On the other hand, reducing PLC1 and PLC1 expressions in db/db islets dramatically attenuated the stimulatory effects of CO on cell function, whereas interfering PLC1 expression had no effects on CO-induced cell function enhancement. Our findings showing that CO elevated [Ca2+]i and enhanced GSIS by activating PLC signaling through PLC1 and PLC1 isoforms in db/db pancreatic cells may suggest an important mechanism by which CO promotes cell function to prevent hyperglycemia. Our study may also provide new insights into the therapy for type II diabetes and offer a potential target for therapeutic applications of CO.
Keywords:
Carbon monoxide; Diabetes; Insulin secretion; Intracellular calcium; Pancreatic cells; Phospholipase C

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