Delayed Ca2+ response to glucose in diabetic GK rat.

The spontaneously diabetic non-obese GK (Goto-Kakizaki) rat exhibits high basal plasma glucose and insulin levels and poor glucose-induced insulin secretion, which makes it a suitable model for non-insulin dependent diabetes mellitus, NIDDM. The aim of this study was to investigate the handling of cytosolic free Ca2+ concentration ([Ca2+]i), the key regulator of insulin secretion, in GK rat single pancreatic islets. For this purpose the influence of high glucose (16.7 mM) and arginine (20 mM) on [Ca2+]i was studied in GK and Wistar rat islets, which served as controls. The data obtained suggest that glucose which through its metabolism generates ATP needed for closure of the KATP channels and membrane depolarization, induces a delayed [Ca2+]i response in the GK rat pancreatic islet. This delay in [Ca2+]i response is likely to result from a defective metabolism of glucose in the diabetic islet.