Intraislet glucagon signaling is critical for maintaining glucose homeostasis by Lu Zhu and others tested whether local glucagon supports insulin release. For human pancreatic islets, a computer-controlled flow system delivered a buffer solution at through a chamber holding 500 pancreatic islets on a nylon filter at . A fraction collector sampled the outgoing fluid. With an amino acid mixture present, the experiment changed glucose from to and compared GLP-1 receptor blockade with fluid lacking the blocker. The readout was released insulin and glucagon: blockade reduced glucose-stimulated insulin release without significantly changing glucagon release. [ref]
Complementary mouse experiments suppressed alpha cell activity using an engineered G protein-coupled receptor. ELISA assays of minute-by-minute effluent samples measured insulin and glucagon concentrations, providing the hormone release readout. Drug-treated control pancreatic islets lacking that engineered receptor checked for drug effects; adding glucagon restored insulin release in the suppressed preparation. Together, blockade and rescue support local signal transduction from alpha cells to beta cells. Isolated pancreatic islets omit intact circulation and nervous input; the human preparation came from five donors, and blocker specificity and donor variation limit generalization. A chamber response does not directly measure whole-body blood glucose control. [ref]
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