Taurine regulates insulin release from pancreatic beta cell lines

Abstract

BackgroundPancreatic 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.MethodsPancreatic β-cell lines Hit-TI5 (Syrian hamster) and Rin-m (rat insulinoma) were used in these studies. Cells were grown to an 80% confluence on uncoated cover glass in RPMI media containing 10% fetal horse serum. The cells were then adapted to a serum-free, glucose free environment for 24 hours. At that time, the cells were treated with either 1 mM glucose, 1 mM taurine, 1 mM glucose + 1 mM taurine, 3 mM glucose, or 3 mM glucose + 1 mM taurine. The cells were examined by confocal microscopy for cytoplasmic levels of insulin.ResultsIn both cell lines, 1 mM glucose had no effect on insulin levels and served as a control. Cells starved of glucose had a significant reduction (p<0.001) in the level of insulin, but this level was significantly higher than all other treatments. As expected, the 3 mM glucose treatment resulted in a statistically lower (p<0.001) insulin level than control cells. Interestingly, 1 mM taurine also resulted in a statistically lower level of insulin (p<0.001) compared to controls when either no glucose or 1 mM glucose was present. Cells treated with 1 mM taurine plus 3 mM glucose showed a level of insulin similar to that of 3 mM glucose alone.ConclusionsTaurine 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 Anti-Inflammatory Effect of Taurine on Cardiovascular Disease

“…Similar studies in alloxan-induced diabetic rabbit models also found taurine to prevent hyperglycemia, exerting a normalizing and protective role in insulin-dependent diabetics [55,56]. In addition, L'Amoreaux et al demonstrated that the uptake of taurine in pancreatic cell lines leads to the alteration of the electrical potential of the beta cells, resulting in decreased intracellular insulin levels [57]. This suggests that taurine may also play a crucial role in regulating insulin release from pancreatic beta cells into the plasma to reduce elevated glucose in healthy people (Figure 1).…”

Herring Milt Protein Hydrolysate Improves Insulin Resistance in High-Fat-Diet-Induced Obese Male C57BL/6J Mice

“…Fish proteins have high levels of taurine, which is reported to help ameliorate hyperglycemia and dyslipidemia by reducing insulin resistance and leptin levels [32,33,34]. Taurine is also reported to have an effect on insulin release from pancreatic β-cells [35]. Moreover, HPH contains a very high level of L-arginine, which has been demonstrated to potentiate glucose-induced insulin secretion mediated by membrane depolarization, which stimulates insulin secretion through protein kinase A- and C-sensitive mechanisms [36].…”

Taurine supplementation preserves hypothalamic leptin action in normal and protein-restricted mice fed on a high-fat diet

“…Taurine (Tau) is a semi-essential amino acid present in high concentrations in the brain and is responsible for the maintenance of intracellular osmotic balance (L'Amoreaux et al 2010). Tau suppresses the activation of the endoplasmic reticulum (ER) stress response in the CNS (Pan et al 2010;Gharibani et al 2013).…”