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

Ročić, Boris; Vučić-Lovrenčić, Marijana; Poje, Nevenka; Poje, Mirko; Bertuzzi, F.

Pregled bibliografske jedinice broj: 422048

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

Ročić, Boris; Vučić-Lovrenčić, Marijana; Poje, Nevenka; Poje, Mirko; Bertuzzi, F.

Uric acid may inhibit glucose-induced insulin secretion via binding to an essential arginine residue in rat pancreatic beta-cells // Bioorganic & medicinal chemistry letters, 15 (2005), 4; 1181-1184 (međunarodna recenzija, članak, znanstveni)

CROSBI ID: 422048 Za ispravke kontaktirajte CROSBI podršku putem web obrasca

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

Autori
Ročić, Boris ; Vučić-Lovrenčić, Marijana ; Poje, Nevenka ; Poje, Mirko ; Bertuzzi, F.

Izvornik
Bioorganic & medicinal chemistry letters (0960-894X) 15 (2005), 4; 1181-1184

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni

Ključne riječi
uric acid; quanidinium urate; glucose-stimulated insulin secretion; arginine; inhibition; pancreatic islets

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

Izvorni jezik
Engleski

Znanstvena područja
Kemija

POVEZANOST RADA

Projekti:
0119613

Ustanove:
Prirodoslovno-matematički fakultet, Zagreb

Profili:

Boris Ročić (autor)