Individual mice can be distinguished by the period of their islet calcium oscillations - Is there an intrinsic islet period that is imprinted in vivo?

Pulsatile insulin secretion in vivo is believed to be derived, in part, from the intrinsic glucose-dependent intracellular calcium concentration ([Ca2+](i)) pulsatility of individual islets. In isolation, islets display fast, slow, or mixtures of fast and slow [Ca2+](i) oscillations. We show that the period of islet [Ca2+](i) oscillations is unique to each mouse, with the islets from an individual mouse demonstrating similar rhythms to one another. Based on their rhythmic period, mice were broadly classified as being either fast (0.65 +/- 0.1 min; n = 6 mice) or slow (4.7 +/- 0.2 min; n = 15 mice). To ensure this phenomenon was not an artifact of islet-to-islet communication, we confirmed that islets cultured in isolation (period: 2.9 +/- 0.1 min) were not statistically different from islets cultured together from the same mouse (3.1 +/- 0.1 min, P > 0.52, n = 5 mice). We also compared pulsatile insulin patterns measured in vivo with islet [Ca2+](i) patterns measured in vitro from six mice. Mice with faster insulin pulse periods corresponded to faster islet [Ca2+](i) patterns, whereas slower insulin patterns corresponded to slower [Ca2+](i) patterns, suggesting that the insulin rhythm of each mouse is preserved to some degree by its islets in vitro. We propose that individual mice have characteristic oscillatory [Ca2+](i) patterns, which are imprinted in vivo through an unknown mechanism.