tisdag 27 juni 2017

Somatostatiini eritys ja tauriini


Pancreatic β-cells release insulin via an electrogenic response triggered by an increase in plasma glucose concentrations. The critical plasma glucose concentration has been determined to be ~3 mM, at which time both insulin and GABA are released from pancreatic β-cells. Taurine, a β-sulfonic acid, may be transported into cells to balance osmotic pressure.
 The taurine transporter (TauT) has been described in pancreatic tissue, but the function of taurine in insulin release has not been established. Uptake of taurine by pancreatic β-cells may alter membrane potential and have an effect on ion currents. If taurine uptake does alter β-cell current, it might have an effect on exocytosis of cytoplasmic vesicle. We wished to test the effect of taurine on regulating release of insulin from the pancreatic β-cell.


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Taurine administration can alter the electrogenic response in β-cell lines, leading to a change in calcium homeostasis and a subsequent decrease in intracellular insulin levels. The consequence of these actions could represent a method of increasing plasma insulin levels leading to a decrease in plasma glucose levels.


The endocrine pancreas is regulated by neurotransmitters, including the use of glutamate and GABA to regulate insulin and glucagon release as well as somatostatin to regulate both α- and β-cell activities. For insulin release, a rise in extracellular glucose to ~3 mM initiates co-release of insulin and GABA [1]. The elevated glucose likely stimulates the release of insulin and GABA from the synapse-like microvesicles (SLMV) through changes in ion currents in β-cells [2,3]. While the insulin is free to move to the circulatory system through the interstitial fluid, GABA binds to GABAA receptors on αcells, causing the hyperpolarization of the α-cells, and inhibiting release of glucagon. Glutamate released from α-cells binds to GluR4 receptors on δ-cells, increasing the release of SST [4]. SST binds either to the SSTR2 receptor on the α-cell or the SSTR1 and/or SSTR5 receptor on the β-cell. SSTR2 activation maintains the GABA-initiated inhibition of glucagon from α-cells, while the SSTR1/5 receptors are responsible for inhibiting insulin release [5].
Taurine (2-aminoethanesulfonic acid) is a sulfur-containing amino acid and is developmentally high in neonates, especially in the brain, and the levels decline to reach stable adult concentrations that are second to those of glutamate in the brain. In the adult, taurine is responsible for maintaining intracellular osmotic balance in a variety of cells examined [6-8]. In the non-obese diabetic mouse model, taurine alters islet development [9]. Previous work done in our laboratory demonstrate that taurine administration during early development in the mouse causes an increase in the number and size of pancreatic islets, without affecting the exocrine portion of the organ [10]. Further, resting plasma glucose levels in these mice were significantly lower than in age-matched controls (manuscript in preparation). When we examined the relative immunoreactivity of insulin, glucagon, and somatostatin in the pancreas of these mice, we found a significant increase in the levels of all three islet markers.
To determine the level at which taurine may interact with the pancreatic β-cells, we set out to test our hypothesis that taurine influences insulin release through its electrogenic transport into the cell. We used immunohistochemistry to address relative intracellular levels of insulin in Hit-T15 (pancreatic β-cell line) and Rin-m (insulinoma) cells.

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