Somatostatin promotes glucose generation of Caoscillations in pancreatic islets both in the absence and presence of tolbutamide.

Many cellular processes, including pulsatile release of insulin, are triggered by increase of cytoplasmic Ca. This study examines how somatostatin affects glucose generation of cytoplasmic Ca oscillations in mouse islets in absence and presence of tolbutamide blockade of the K channels. Ca was measured with dual wavelength microflurometry in isolated islets loaded with the indicator Fura-2.

Sulfonylurea Blockade of KATP Channels Unmasks a Distinct Type of Glucose-Induced Ca2+ Decrease in Pancreatic β-Cells.

Objectives: This study aimed to explore how sulfonylurea blockade of KATP channels affects the early Ca signals for glucose generation of insulin release.

Methods: Cytoplasmic Ca was measured with ratiometric microfluorometry in isolated mouse islets loaded with Fura-PE3.

Results: After sulfonylurea blockade of the KATP channels (50 μM-1 mM tolbutamide or 1 μM-1 mM gliclazide), increase of glucose from 3 to 20 mM resulted in suppression of elevated Ca during a 3- to 5-minute period.

Small Mouse Islets Are Deficient in Glucagon-Producing Alpha Cells but Rich in Somatostatin-Secreting Delta Cells.

Small and big mouse islets were compared with special reference to their content of glucagon-producing α-cells and somatostatin-producing δ-cells. Areas stained for glucagon and somatostatin were measured in the largest cross section of small (diameter < 60 μm) and big (diameter > 100 μm) islets. Comparison of the areas indicated proportionally more δ- than α-cells in the small islets.

Activation of alpha adrenergic and muscarinic receptors modifies early glucose suppression of cytoplasmic Ca(2+) in pancreatic β-cells.

Elevation of glucose induces transient inhibition of insulin release by lowering cytoplasmic Ca(2+) ([Ca(2+)]i) below baseline in pancreatic β-cells. The period of [Ca(2+)]i decrease (phase 0) coincides with increased glucagon release and is therefore the starting point for antisynchronous pulses of insulin and glucagon. We now examine if activation of adrenergic α2A and muscarinic M3 receptors affects the initial [Ca(2+)]i response to increase of glucose from 3 to 20mM in β-cells situated in mouse islets.

Glucose-induced inhibition of insulin secretion.

Increase in glucose is known to elevate the concentration of cytoplasmic Ca(2+) ([Ca(2+) ]i ) in pancreatic β-cells and stimulate insulin secretion. However, rise of glucose can also lower [Ca(2+) ]i and inhibit insulin release. In the present review, we examine the mechanisms for this inhibition and highlight its importance for the healthy β-cell and the development of diabetes.