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Fig. 2 | Journal of Translational Medicine

Fig. 2

From: β-cell mitochondria in diabetes mellitus: a missing puzzle piece in the generation of hPSC-derived pancreatic β-cells?

Fig. 2

adapted from Cantley et al. [112]

Overview of low glucose and high glucose-stimulated insulin secretion. At basal levels of blood glucose (left panel), the ATP-sensitive K+ channels (KATP channels) in pancreatic β-cells remain open, maintaining membrane hyperpolarization, Ca2+ channel closure and inhibiting insulin secretion. A rise in blood glucose (right panel) induces oxidative phosphorylation and ATP production, resulting in the closure of KATP channels, plasma membrane depolarization, calcium influx leading to increased cytosolic Ca2+ that triggers insulin exocytosis: a so-called classical KATP channel-dependent pathway

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