Fig. 8 | Nature Communications

Fig. 8

From: Insulin inhibits glucagon release by SGLT2-induced stimulation of somatostatin secretion

Fig. 8

Schematic summarising the effects of insulin in δ cells. Relationship between SGLT2-mediated glucose uptake and δ-cell electrical activity, Ca2+ entry, Ca2+-induced Ca2+ release (CICR) and somatostatin release. Insulin stimulates SGLT2 activity. The operation of SGLT2 is electrogenic Na+-dependent glucose uptake mediated by SGLT2 gives rise to a small depolarising current and may (in some cells with sufficiently high SGLT2 expression and/or low KATP channel activity) trigger electrical activity (action potential firing). The associated increase in cytoplasmic Ca2+ ([Ca2+]i) leads to intracellular Ca2+ mobilisation by activation of ryanodine receptors (RyRs) and Ca2+-induced Ca2+ release (CICR). In addition to SGLT2, the δ cells also express the glucose transporters GLUT1 and GLUT3. Glucose uptake via these transporters accounts for 99% of glucose uptake. Metabolism of glucose leads to KATP channel closure, membrane depolarisation, electrical activity and CICR

Back to article page