Pancreatic β-Cell Response to Increased Metabolic Demand and to Pharmacologic Secretagogues Requires EPAC2A

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FIG. 6.
FIG. 6.

EPAC2A ablation impairs GSIS augmentation in response to free fatty acid 1/GRP40 activation. A: Perifusion studies of PMAP-treated islets GSIS augmentation in WT islets, which is blunted in EPAC2A KO islets mainly in the acute phase (40–42 min) after glucose stimulus to the islets, while later time points show similar insulin secretion in WT and EPAC2A KO islets. B and C: Islet intracellular calcium dynamic changes detected with the Fura-2 method in PMAP-treated WT and EPAC2A KO islets. B: Islets maintained in 3 mmol/L glucose show no differences in intracellular calcium levels. C: Increasing glucose levels from 3 to 10 mmol/L at time 0 min elicits an increase in intracellular calcium signal in WT islets. EPAC2A KO islets show a blunted early (0–10 min) rise in glucose-stimulated intracellular calcium, which, at later time points (10–20 min), is similar in both groups. WT is represented in gray circles; EPAC2A KO is represented in black circles. Results are shown as mean ± SEM of studies performed at least in triplicate. *P < 0.05.

This Article

  1. Diabetes vol. 62 no. 8 2796-2807