摘要

Islet non-beta-cells, the - - and pancreatic polypeptide cells (PP-cells), are important components of islet architecture and intercellular communication. In -cells, glucagon is found in electron-dense granules; granule exocytosis is calcium-dependent via P/Q-type Ca2+-channels, which may be clustered at designated cell membrane sites. Somatostatin-containing -cells are neuron-like, creating a network for intra-islet communication. Somatostatin 1-28 and 1-14 have a short bioactive half-life, suggesting inhibitory action via paracrine signaling. PP-cells are the most infrequent islet cell type. The embryologically separate ventral pancreas anlage contains PP-rich islets that are morphologically diffuse and -cell deficient. Tissue samples taken from the head region are unlikely to be representative of the whole pancreas. PP has anorexic effects on gastro-intestinal function and alters insulin and glucagon secretion. Islet architecture is disrupted in rodent diabetic models, diabetic primates and human Type 1 and Type 2 diabetes, with an increased -cell population and relocation of non--cells to central areas of the islet. In diabetes, the transdifferentiation of non--cells, with changes in hormone content, suggests plasticity of islet cells but cellular function may be compromised. Understanding how diabetes-related disordered islet structure influences intra-islet cellular communication could clarify how non--cells contribute to the control of islet function.

  • 出版日期2015-8