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• W2000494473 abstract "To demonstrate an involvement of ATP-sensitive potassium (K(ATP)) channel-independent pathways in the first phase of glucose-stimulated insulin secretion (GSIS) from pancreatic beta cells, the time course of GSIS from MIN6 cells was analyzed at 30-s sample intervals. GSIS was biphasic with the first phase being observed 120 to 390 s after glucose addition, peaking at 180 s, and with a shoulder at 240 to 330 s. Both 10 microM diazoxide and 3 microM verapamil completely inhibited tolbutamide- or glibenclamide-induced insulin secretion and suppressed the peak of the first phase of GSIS, but did not result in complete suppression. The shoulder following the peak was suppressed by 1 muM dantrolene. The peak, but not shoulder, disappeared under the extracellular Ca2+-free condition. A significant amount of insulin secretion remained even in the combined presence of verapamil and dantrolene. The Na+ channel blocker tetrodotoxin (30 nM) nearly completely inhibited the first phase release. These results suggest that the first phase of GSIS from MIN6 cells depends on both Ca2+-dependent and -independent mechanisms. The former mechanism includes the extracellular Ca2+ influx via L-type voltage-dependent calcium channel and intracellular Ca2+ release from endoplasmic reticulum via ryanodine receptors, and the latter mechanism involves the pathways associated with Na+ channels." @default.
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• W2000494473 date "2006-01-01" @default.
• W2000494473 modified "2023-10-16" @default.
• W2000494473 title "First Phase of Glucose-Stimulated Insulin Secretion From MIN 6 Cells Does Not Always Require Extracellular Calcium Influx" @default.
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• W2000494473 doi "https://doi.org/10.1254/jphs.fp0060057" @default.
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