Ball, AJ, Flatt, Peter and McClenaghan, Neville (2000) Stimulation of insulin secretion in clonal BRIN-BD11 cells by the imidazoline derivatives KU14R and RX801080. PHARMACOLOGICAL RESEARCH, 42 (6). pp. 575-579. [Journal article]
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The imidazoline derivatives KU14R and RX801080 have each been reported to antagonize imidazoline-stimulated insulin secretion. This study investigated the effects of a range of concentrations of both KU14R and RX801080 on insulin secretion from the clonal pancreatic beta cell line, BRIN-BD11, In the presence of a stimulatory (8.4 mM) glucose concentration, both KU14R (50-200 muM; P<0.01 to P<0.001) and RX801080 (50-200 muM; P < 0.01 to P < 0.001) were found to dose-dependently stimulate insulin secretion. The imidazoline efaroxan (200 muM) stimulated insulin secretion (P < 0.001) from BRIN-BD11 cells. This insulinotropic effect was significantly augmented by KU14R (100-200 muM; P < 0.01 to P < 0.001) and RX801080 (200 muM; P < 0.05). Insulin secretion from BRIN-BD11 cells was also stimulated by the novel guanidine derivative BTS 67 582 (200 >muM; P < 0.001). This secretagogue action was augmented both by KU14R (25-200 muM; P < 0.001) and by RX801080 (25-200 mUM; P <; 0.05 to P < 0.001). It is concluded that, rather than acting as antagonists of imidazoline-induced insulin secretion, the imidazoline derivatives KU14R and RX801080 are themselves potent insulinotropic agents. (C) 2000 Academic Press.
|Item Type:||Journal article|
|Faculties and Schools:||Faculty of Life and Health Sciences|
Faculty of Life and Health Sciences > School of Biomedical Sciences
|Research Institutes and Groups:||Biomedical Sciences Research Institute|
Biomedical Sciences Research Institute > Diabetes
|Deposited By:||Professor Peter Flatt|
|Deposited On:||14 Jan 2010 09:34|
|Last Modified:||15 Jun 2011 10:10|
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