The Cells of the Islets of Langerhans

Abstract

Islets of Langerhans are islands of endocrine cells scattered throughout the pancreas. A number of new studies have pointed to the potential for conversion of non-β islet cells in to insulin-producing β-cells to replenish β-cell mass as a means to treat diabetes. Understanding normal islet cell mass and function is important to help advance such treatment modalities: what should be the target islet/β-cell mass, does islet architecture matter to energy homeostasis, and what may happen if we lose a particular population of islet cells in favour of β-cells? These are all questions to which we will need answers for islet replacement therapy by transdifferentiation of non-β islet cells to be a reality in humans. We know a fair amount about the biology of β-cells but not quite as much about the other islet cell types. Until recently, we have not had a good grasp of islet mass and distribution in the human pancreas. In this review, we will look at current data on islet cells, focussing more on non-β cells, and on human pancreatic islet mass and distribution.

Keywords: diabetes; endocrine; ghrelin; glucagon; insulin; islets of Langerhans; pancreas; pancreatic polypeptide; somatostatin.

Figure 1

Schematic diagram showing the interdependency of islet cells. Evidence in the literature points to the possibility of the transdifferentiation (solid black arrows) of α-cells (red circle) via stimulation by gamma aminobutyric acid (GABA), and δ-cells (yellow circle) into insulin-containing β (like)-cells (blue circle). It is currently unclear whether the replenishment of β-cells from the transdifferentiation of α-cells is able to replace hub β-cells (light blue circle) which influence (yellow arrows) the function of other β-cells. Somatostatin, released from δ-cells, can inhibit the release of glucagon, insulin, and pancreatic polypeptide from α-, β-, and PP cells (green circle), respectively. Pancreatic polypeptide, released from PP cells, can inhibit the release of glucagon. Ghrelin, released from ghrelin-positive islet cells (purple circle), can inhibit insulin and somatostatin secretion.