Uric acid may inhibit glucose-induced insulin secretion via binding to an essential arginine residue in rat pancreatic beta-cells.
Boris Rocić, Marijana Vucić-Lovrencić, Nevenka Poje, Mirko Poje, Federico Bertuzzi
Index: Bioorg. Med. Chem. Lett. 15 , 1181-4, (2005)
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Abstract
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 beta-cell receptor is probably involved in the blocking glucose signal transduction.
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