The role of preproglucagon peptides in regulating β-cell morphology and responses to streptozotocin-induced diabetes

The study examined the role and source of Gcg peptides in β-cell function and in response to STZ-induced hyperglycemia. In animals not treated with STZ, GcgNull mice had increased pancreas mass via both α- and β-cell hyperplasia and reactivation of Gcg in the intestine normalised β- but not α-cell mass, while pancreatic reactivation normalised both β- and α-cell mass. GcgNull and GcgΔIntest mice maintained higher β-cell mass after treatment with STZ than control and GcgΔPanc mice. Interestingly, mice with intestinal Gcg reactivated in adulthood had impaired insulin response to KCl. The study surmises that the expansion of β-cell mass in the GcgNull mice compensated for decreased individual β-cell insulin secretion, sufficient to normalise glucose under physiological conditions and conferred some protection after STZ-induced diabetes.