Taurine supplementation induces hyperinsulinemia and neuronal hyperexcitability.

Abstract

In this study we examined the role of taurine in mediating increased insulin production and secretion by the pancreas and the functional relevance for plasma glucose homeostasis and brain excitability. One-month-old FVB/NJ males were supplemented with taurine in drinking water (0.05 % w/v) for 4 weeks. At that time, mice were sacrificed and pancreases processed for histology and immunohistochemistry. Additional mice were subjected to a glucose tolerance test (7.5 mg/kg BW) after 12 h fasting. We found that taurine supplementation resulted in a significant increase in the number and size of the islets of Langerhans. Taurine-fed mice were slightly hypoglycemic prior to glucose injection and showed a significantly reduced plasma glucose at 30 and 60 min post-glucose injection when compared to control mice. Concomitant with the increased islets size and glucose tolerance observed in taurine-fed mice there was an increase in insulin, glucagon and somatostatin immunoreactivity in the islets. Previously, we reported that taurine supplementation induces biochemical changes in the GABAergic system in the brain. Those studies show that taurine-fed mice are hyperexcitable, have reduced GABAA receptors expression and increased GAD and somatostatin expression in the brain. In this study, we also found that taurine-fed mice had a significant increase in insulin receptor (IR) immunoreactivity in all brain regions examined. Circulating insulin crosses the blood brain barrier through a saturable mechanism. We propose that increased insulin production and secretion in taurine-fed mice caused increased activation of the central IR and may be partially responsible for the increased neuronal excitability observed in taurine supplemented mice.