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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 glucose… Expand
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 of… Expand
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 by… Expand
Regulation of insulin release by calcium.
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 was… Expand
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 nM… Expand
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 at… Expand
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 mechanisms… Expand
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 to… Expand
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 intact… Expand