Investigation of the effects of taurine on the pancreatic islets overexpressing glucokinase

• Grant number: 13/25071-8
• Support Opportunities: Scholarships abroad - Research Internship - Doctorate
• Start date: May 01, 2014
• End date: April 30, 2015
• Field of knowledge: Biological Sciences - Biochemistry - Metabolism and Bioenergetics
• Principal Investigator: Everardo Magalhães Carneiro
• Grantee: Renato Chaves Souto Branco
• Supervisor: Antonio Luis Cuesta-Muñoz
• Host Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
• Institution abroad: University of Copenhagen, Copenhagen, Denmark
• Associated to the scholarship: 11/20196-1 - INVOLVEMENT OF METABOLIC COUPLING FACTORS ON INSULIN SECRETION PROCESS IN UNDERNOURISHED MICE SUBMITED TO EXPERIMENTAL OBESITY, BP.DR

Abstract

Glucose is the major stimulus for insulin secretion. Obesity and Diabetes Mellitus are related to disrupted energy homeostasis, leading to pancreatic beta cell dysfunction. The glycolytic enzyme glucokinase (GK) is a key regulator of insulin secretion in the pancreatic beta cells, playing a critical role in the maintenance of the physiological glucose set point. Detailed morphometric evaluation of the pancreatic tissue from patients with naturally occurring activating GK (NAGCK) mutations, revealed significantly enlarged and well-formed islets with increased beta cell proliferation and heightened metabolic rate. Besides this mutation, the glycolytic flux may be increased by nutritional interventions such as amino acid supplementation. Taurine is a sulfur containing amino acid involved on the regulation of beta cell physiology. It was reported that taurine supplementation induces an increase on GK and PDX-1 gene expression, which could contribute for the increased insulin secretion capacity. We hypothesize that interventions aimed at increasing GK expression in wild type mice islets would lead to increased beta cell proliferation and metabolic capacity which could be beneficial in situations of disrupted energy homeostasis and poor islet function. Likewise, this approach can provide us important information about the relationship of the activation of GK and proliferation of mice insulin secreting cells in the background of amino acid supplementation such as taurine. (AU)