Pancreatic α cell

The principal level of control on glycaemia by the islet of Langerhans depends largely on the coordinated secretion of glucagon and insulin by α- and β-cells respectively. Both cell types respond oppositely to changes in blood glucose concentration: while hypoglycaemic conditions induce α-cell secretion, β-cells release insulin when glucose levels increase. Insulin and glucagon have opposite effects on glycaemia as well as on the metabolism of nutrients. Insulin acts mainly on muscle, liver and adipose tissue with an anabolic effect, inducing the incorporation of glucose into these tissues and its accumulation as glycogen and fat. By contrast, glucagon induces a catabolic effect, mainly by activating liver glycogenolysis and gluconeogenesis, which results in the release of glucose to the bloodstream. An abnormal function of these cells can generate failures in the control of glycaemia, which can lead to the development of diabetes. Actually, diabetes is associated with disorders in the normal levels of both insulin and glucagon. An excess of glucagon plasma levels relative to those of insulin can be determinant in the higher rate of hepatic glucose output, which seems to be critical in maintaining hyperglycaemia in diabetic patients