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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Selectivity of prandial glucose regulators: nateglinide, but not repaglinide, accelerates exocytosis in rat pancreatic A-cells.

The effects of the two prandial glucose regulators, repaglinide and nateglinide, on ATP-sensitive K(+) (K(ATP)) channel activity, membrane potential and exocytosis in single rat pancreatic A-cells were investigated using the patch-clamp technique. K(ATP) channel activity was reversibly blocked by repaglinide (K(d)=22 nM) and nateglinide (K(d)=410 nM) and this was associated with membrane depolarisation and initiation of electrical activity. The effect of repaglinide and nateglinide on stimulation of glucagon secretion by direct interference with the exocytotic machinery was investigated by the use of capacitance measurements. Nateglinide, but not repaglinide, at concentrations similar to those required to block K(ATP) channels potentiated Ca(2+)-evoked exocytosis 3-fold. In alphaTC1-9 glucagonoma cells addition of nateglinide, but not repaglinide, was associated with stimulation of glucagon secretion. These results indicate that the fast-acting insulin secretagogue nateglinide is glucagonotropic primarily by stimulating Ca(2+)-dependent exocytosis.[1]

References

  1. Selectivity of prandial glucose regulators: nateglinide, but not repaglinide, accelerates exocytosis in rat pancreatic A-cells. Bokvist, K., Hoy, M., Buschard, K., Holst, J.J., Thomsen, M.K., Gromada, J. Eur. J. Pharmacol. (1999) [Pubmed]
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