Uric acid may inhibit glucose-induced insulin secretion via binding to an essential arginine residue in rat pancreatic β-cells

Uric acid (1a) suppresses basal insulin release in isolated rat pancreatic islets and inhibition of glucose-stimulated insulin secretion (GSIS) occurs right at hyperuricaemic levels ( 0.4 mM). Conversely, 1 mM guanidinium urate (2a) was completely ineffective, strongly suggesting that binding to an essential arginine residue triggers the inhibitory effect. A specific recognition of 1a molecule at the crucial β-cell receptor is probably involved in the blocking glucose signal transduction.