= Islet perifusion experiment
<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 $1\,\mathrm{ml}/\mathrm{min}$ through a chamber holding 500 <pancreatic islets> on a nylon filter at $37\,{}^\circ\mathrm C$. A fraction collector sampled the outgoing fluid. With an <amino acid> mixture present, the experiment changed <glucose> from $3$ to $16.7\,\mathrm{mM}$ 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. <Intraislet glucagon signaling is critical for maintaining glucose homeostasis by Lu Zhu and others>{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. <Intraislet glucagon signaling is critical for maintaining glucose homeostasis by Lu Zhu and others>{ref}
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