The role of insulin and hyperglycemia in the delta cell transdifferentiation to beta cell in streptozotocin diabetic mice

• Grant number: 15/10705-7
• Support Opportunities: Scholarships in Brazil - Post-Doctoral
• Start date: August 01, 2015
• End date: September 30, 2020
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Agreement: Coordination of Improvement of Higher Education Personnel (CAPES)
• Principal Investigator: Antonio Carlos Boschiero
• Grantee: Sandra Mara Ferreira
• Host Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
• Associated research grant: 15/12611-0 - Molecular mechanisms involved in pancreatic beta cell disfunction and dead in diabetes mellitus: strategies for the inhibition of these processes and restoration of the insular mass, AP.TEM
• Associated scholarship(s): 19/04281-0 - The role of Insulin on pancreatic delta cell development, BE.EP.PD

Abstract

Diabetes Mellitus (DM) is characterized by chronic hyperglycemia, resulting from a partial or total reduction of insulin, due the partial or total destruction of pancreatic beta cell mass. Recover beta cell mass and consequently the insulin secretion is crucial for the treatment of DM. It was demonstrated that non-beta cells of pancreas (endocrine and non-endocrine) have the ability to reprogram and change their phenotype to express insulin, recovering beta cell mass. Among these, the delta cells are a possible source of new beta cells in young mice. In mice with depletion of beta cells, dedifferentiated delta cells entered in the cell cycle and after, differentiated in beta cells. However, the mechanism that controls these delta cells modifications is not yet understood. With this project we intend to clarify the mechanisms underlining delta cell dedifferentiation as well as the factors that participate in the remodeling of these cells toward beta cells, in a model of beta cell depletion. (AU)