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In GLUTag cells, DCA-stimulated GLP-1 secretion was significantly inhibited by H-89, a PKA inhibitor, and/or ESI-09, inhibitors of EPAC1, and EPAC2, in the low-glucose (0.1 mM) state (Fig
The authors proposed that the increased GLP-1 levels potentiated the insulin surge and contributed to the subsequent hypoglycemia
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