  Major part of a pancreatic islet is composed of beta cells that secrete
insulin, a key hormone regulating influx of nutrients into all cells in a
vertebrate organism to support nutrition, housekeeping or energy storage. Beta
cells constantly communicate with each other using both direct, short-range
interactions through gap junctions, and paracrine long-range signaling.
However, how these cell interactions shape collective sensing and cell behavior
in islets that leads to insulin release is unknown. When stimulated by specific
ligands, primarily glucose, beta cells collectively respond with expression of
a series of transient Ca$^{2+}$ changes on several temporal scales. Here we
analyze a set of Ca$^{2+}$ spike trains recorded in acute rodent pancreatic
tissue slice under physiological conditions. We found strongly correlated
states of co-spiking cells coexisting with mostly weak pairwise correlations
widespread across the islet. Furthermore, the collective Ca$^{2+}$ spiking
activity in islet shows on-off intermittency with scaling of spiking
amplitudes, and stimulus dependent autoassociative memory features. We use a
simple spin glass-like model for the functional network of a beta cell
collective to describe these findings and argue that Ca$^{2+}$ spike trains
produced by collective sensing of beta cells constitute part of the islet
metabolic code that regulates insulin release and limits the islet size.
