Abstract
Intrauterine and early life nutritional deficiency favors metabolic and cardiovascular disorders such as hypertension and insulin resistance. In this context, insulinotropic amino acids may act as a complementary therapy. Currently our group investigates the effects of amino acids depletion in vitro on insulin secretion and action. So far, we have reported that the in vitro withdrawal of all amino acids reduces insulin secretion in a similar manner observed in the in vivo model of protein malnourished rodents. However, the individual role of different amino acids on the control of insulin secretion and action has not been established yet. Taurine is an amino acid synthesized from cysteine involved in several intracellular processes such as cellular volume and Ca2+ flux control. Among potential insulinotropic and insulinomimetic amino acids, taurine action on metabolic and endothelial homeostasis is detached in several studies. Although evidence point to the relevance of this amino acid, there are unanswered questions regarding the mechanisms by which its action occurs. Therefore, this proposal aims to investigate the intracellular mechanisms associated with insulinotropic, insulinomimetics and endothelial effects of taurine. To achieve these objectives, it will be employed in vitro cellular lines and animal protein malnutrition models to the study insulin, glucagon and somatostatin secretion and action focusing on dinamic oscilations of Ca2+, ATP, NAD(P)H and mitochondrial membrane potencial (Èm) in pancreatic islets, hepatocytes, miotubules and endothelial cells submitted to an in vitro protocol of protein restriction. (AU)
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