Uric acid may inhibit glucose-induced insulin secretion via binding to an essential arginine residue in rat pancreatic beta-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 beta-cell receptor is probably involved in the blocking glucose signal transduction.
Rocić
Boris
B
University Clinic Vuk Vrhovac, Medical Faculty, Dugi dol 4a, 10000 Zagreb, Croatia.
Vucić-Lovrencić
Marijana
M
Poje
Nevenka
N
Poje
Mirko
M
Bertuzzi
Federico
F
D000818:Animals; D001120:Arginine / Q000378:metabolism*; D005947:Glucose / Q000494:pharmacology*; D033461:Hyperuricemia; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000166:cytology / Q000378:metabolism*; D011485:Protein Binding; D051381:Rats; D013329:Structure-Activity Relationship; D014527:Uric Acid / Q000494:pharmacology*
D007328:Insulin; D014527:Uric Acid; D001120:Arginine; D005947:Glucose