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Glucose‐stimulated signaling pathways in biphasic insulin secretion
Glucose‐stimulated biphasic insulin secretion involves at least two signaling pathways, the KATP channel‐dependent and KATP channel‐independent pathways, respectively. In the former, enhanced glucoseExpand
  • 409
  • 24
Mechanisms of inhibition of insulin release.
  • G. Sharp
  • Biology, Medicine
  • The American journal of physiology
  • 1 December 1996
Several agonists including norepinephrine, somatostatin, galanin, and prostaglandins inhibit insulin release. The inhibition is sensitive to pertussis toxin, indicating the involvement ofExpand
  • 198
  • 11
Triggering and augmentation mechanisms, granule pools, and biphasic insulin secretion.
The insulin secretory response by pancreatic beta-cells to an acute "square wave" stimulation by glucose is characterized by a first phase that occurs promptly after exposure to glucose, followed byExpand
  • 242
  • 10
  • Open Access
Regulation of insulin release by calcium.
  • 676
  • 9
Stimulation of insulin release by glucose is associated with an increase in the number of docked granules in the beta-cells of rat pancreatic islets.
Electron microscopy and quantitative stereological techniques were used to study the dynamics of the docked granule pool in the rat pancreatic beta-cell. The mean number of granules per beta-cell wasExpand
  • 87
  • 8
  • Open Access
A Wortmannin-sensitive Signal Transduction Pathway Is Involved in the Stimulation of Insulin Release by Vasoactive Intestinal Polypeptide and Pituitary Adenylate Cyclase-activating Polypeptide (*)
Vasoactive intestinal polypeptide (VIP), pituitary adenylate cyclase-activating polypeptide-27 (PACAP-27), and PACAP-38 stimulated insulin release with EC values of 0.15, 0.15, and 0.06 nMExpand
  • 105
  • 5
Glucose-induced insulin release in islets of young rats: time-dependent potentiation and effects of 2-bromostearate.
The development of glucose-stimulated insulin release and time-dependent potentiation (TDP) has been studied in isolated islets from 7-, 14-, and 21-day-old and 3-mo-old rats. Responses were small atExpand
  • 71
  • 5
Hypothesis: one rate-limiting step controls the magnitude of both phases of glucose-stimulated insulin secretion.
  • S. G. Straub, G. Sharp
  • Medicine, Biology
  • American journal of physiology. Cell physiology
  • 1 September 2004
The biphasic secretory response of pancreatic beta-cells to abrupt and sustained exposure to glucose is well documented. Some of the ATP-sensitive K(+) (K(ATP)) channel-dependent mechanismsExpand
  • 77
  • 5
  • Open Access
Evolving insights regarding mechanisms for the inhibition of insulin release by norepinephrine and heterotrimeric G proteins.
Norepinephrine has for many years been known to have three major effects on the pancreatic β-cell which lead to the inhibition of insulin release. These are activation of K(+) channels toExpand
  • 44
  • 5
  • Open Access
Hyperinsulinism of infancy: the regulated release of insulin by KATP channel-independent pathways.
Hyperinsulinism of infancy (HI) is a congenital defect in the regulated release of insulin from pancreatic beta-cells. Here we describe stimulus-secretion coupling mechanisms in beta-cells and intactExpand
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  • Open Access