Homotypic cell contact enhances insulin but not glucagon secretion

Intra-islet interactions influence β-cell function, and disruption of islet architecture results in a reduction in glucose-induced insulin secretion, whereas re-aggregation improves secretory responsiveness. Our studies on MIN6 cells have shown that by configuring β-cells as three-dimensional islet-like structures there is a marked improvement in glucose-induced insulin secretion compared to that of their monolayer equivalents. In the present study, we have used the mouse glucagon-secreting αTC1 cell line to see whether homotypic interactions are important in the regulation of glucagon secretion from α-cells. We found no significant difference in the secretory responses of αTC1 cells maintained as monolayers or as cell clusters. We also found that different cell adhesion molecules are involved in cell interactions between α- and β-cells; MIN6 cells express ECAD, whereas αTC1 cells express NCAM. ECAD is necessary for cell cluster formation by MIN6 cells but not by αTC1 cells, whereas NCAM is not needed for the formation of cell clusters in either cell line.