ncs-382 and 3-chloropropionic-acid

Hypersecretion of glucagon from pancreatic α-cells strongly contributes to diabetic hyperglycemia. Moreover, failure of α-cells to increase glucagon secretion in response to falling blood glucose concentrations compromises the defense against hypoglycemia, a common complication in diabetes therapy. However, the mechanisms underlying glucose regulation of glucagon secretion are poorly understood and likely involve both α-cell-intrinsic and intraislet paracrine signaling. Among paracrine factors, glucose-stimulated release of the GABA metabolite γ-hydroxybutyric acid (GHB) from pancreatic β-cells might mediate glucose suppression of glucagon release via GHB receptors on α-cells. However, the direct effects of GHB on α-cell signaling and glucagon release have not been investigated. Here, we found that GHB (4-10 μm) lacked effects on the cytoplasmic concentrations of the secretion-regulating messengers Ca

Topics: Adult; Aged; Aged, 80 and over; Animals; Benzocycloheptenes; Cells, Cultured; Enzyme Inhibitors; Female; GABA Agents; Glucagon; Glucagon-Secreting Cells; Glucose; Humans; Male; Mice; Mice, Inbred C57BL; Middle Aged; Propionates; Sodium Oxybate; Vigabatrin