The phenotype of mice largely or totally depleted in Cx36 shows several beta cell alterations which are typical of glycemia disorders, including loss of circulating insulin oscillations, glucose intolerance, increased basal secretion, decreased first and second phase of glucose-induced insulin secretion, and increased beta cell apoptosis [51, 62, 235, 248, 252, 256]. Here, INS is linked to Glucose intolerance.