Regulation of Ca²⁺ Transport by Insulin and Taurine

Abstract

In 1983 Lampson et al. ¹⁶ and Tokunaga et al. ³¹ introduced the concept that an interaction must exist between the actions of taurine and those of insulin. The initial studies examining this question focused on the metabolic actions of insulin. Tokunaga et al. ³¹ found that taurine suppressed insulin secretion in nondiabetic pancreatic islets, suggesting that taurine might serve as a physiological regulator of insulin secretion and plasma glucose levels. They also found that taurine levels increased significantly in diabetic islets, implying that taurine might contribute to the state of hypoinsulinemia and hyperglycemia. Lampson et al. ¹⁶ also concluded that taurine influenced plasma glucose levels, but their studies linked the hypoglycemic actions of taurine to a potentiation of insulin-mediated glucose uptake. Lampson et al. ¹⁶ also reported that taurine promoted several other insulin sensitive reactions, implying that taurine either facilitated the interaction of insulin with its receptor or increased the production of a putative second messenger of insulin. Subsequent studies revealed that taurine could interact directly with the insulin receptor^{15, 20}. This interaction appeared to be quite specific since insulin was capable of displacing taurine from its binding sites²⁰. Based on these data, Maturo and Kulakowski²⁰ suggested that taurine might exhibit insulin-mimetic activity. However, this notion is inconsistent with a recent observation by Schaffer et al. ³⁰ that insulin, but not taurine, could stimulate Na⁺-Ca²⁺ exchanger activity. Yet, the studies by Schaffer et al. ³⁰ did not address the possibility that taurine might function as a general modulator of insulin action.