Taurine’s Effects on the Neuroendocrine Functions of Pancreatic β Cells
Taurine plays significant physiological roles, including those involved in neurotransmission. Taurine is a potent γ-aminobutyric acid (GABA) agonist and alters cellular events via GABAA receptors. Alternately, taurine is transported into cells via the high affinity taurine transporter (TauT), where it may also play a regulatory role. We have previously demonstrated that treatment of Hit-T15 cells with 1 mM taurine for 24 h significantly decreases insulin and GABA levels. We have also demonstrated that chronic in vivo administration of taurine results in an up-regulation of glutamic acid decarboxylase (GAD), the key enzyme in GABA synthesis. Here, we wished to test if administration of 1 mM taurine for 24 h may increase release of another β cell neurotransmitter somatostatin (SST) and also directly impact up-regulation of GAD synthesis. Treatment with taurine did not significantly alter levels of SST (p > 0.05) or GAD67 (p > 0.05). This suggests that taurine does not directly affect SST release, nor does it directly affect GAD synthesis. Taken together with our observation that taurine does promote GABA release via large dense-core vesicles, the data suggest that taurine may alter membrane potential, which in turn would affect calcium flux. We show here that 1 mM taurine does not alter intracellular Ca2+ concentrations from 20 to 80 s post treatment (p > 0.05), but does increase Ca2+ flux between 80 and 200 s post-treatment (p < 0.005). This suggests that taurine may induce a biphasic response in β cells. The initial response of taurine via GABAA receptors hyperpolarizes β cell and sequesters Ca2+. Subsequently, taurine may affect Ca2+ flux in long term via interaction with KATP channels.
KeywordsGlycine Cysteine Retina Polypeptide Paraformaldehyde
Glutamic acid decarboxylase
Large dense-core vesicles
We thank Jonathan Blaize and Janto Tachjadi for assistance with the confocal microscopy. Support for the confocal microscope comes from the National Science Foundation (DBI 0421046). Support also from the Professional Staff Congress of the City University of New York. We would also like to thank the Organizing Committee of the 18th International Taurine Meeting for the scientific and social programs and the participants that made this a memorable conference.
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