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- Title
The novel imidazoline compound BL11282 potentiates glucose-induced insulin secretion in pancreatic beta-cells in the absence of modulation of K(ATP) channel activity.
- Authors
Efanov, Alexander M.; Zaitsev, Sergei V.; Mest, Hans-Juergen; Raap, Achim; Appelskog, Ioulia B.; Larsson, Olof; Berggren, Per-Olof; Efendic, Suad; Efanov, A M; Zaitsev, S V; Mest, H J; Raap, A; Appelskog, I B; Larsson, O; Berggren, P O; Efendic, S
- Abstract
The insulinotropic activity of the novel imidazoline compound BL11282 was investigated. Intravenous administration of BL11282 (0.3 mg x kg(-1) x min(-1)) to anesthetized rats did not change blood glucose and insulin levels under basal conditions, but produced a higher increase in blood insulin levels and a faster glucose removal from the blood after glucose infusion. Similarly, in isolated Wistar rat pancreatic islets, 0.1-100 micromol/l BL11282 potently stimulated glucose-induced insulin secretion but did not modulate basal insulin secretion. Unlike previously described imidazolines, BL11282 did not block ATP-dependent K+ channels. Furthermore, the compound stimulated insulin secretion in islets depolarized with high concentrations of KCl or permeabilized with electric shock. Insulinotropic activity of BL11282 was dependent on activity of protein kinases A and C. In pancreatic islets from spontaneously diabetic GK rats, the imidazoline compound restored the impaired insulin response to glucose. In conclusion, the imidazoline BL11282 constitutes a new class of insulinotropic compounds that exerts an exclusive glucose-dependent insulinotropic activity in pancreatic islets by stimulating insulin exocytosis.
- Subjects
IMIDAZOLINES; INSULIN; PANCREATIC beta cells; POTASSIUM channels; SECRETION
- Publication
Diabetes, 2001, Vol 50, Issue 4, p797
- ISSN
0012-1797
- Publication type
journal article
- DOI
10.2337/diabetes.50.4.797