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The role of long non-coding RNAs in insulin resistance and type 2 diabetes

Grant number: 20/04149-2
Support type:Scholarships abroad - Research Internship - Doctorate
Effective date (Start): March 01, 2021
Effective date (End): February 28, 2022
Field of knowledge:Health Sciences - Physical Education
Principal researcher:José Rodrigo Pauli
Grantee:Vitor Rosetto Muñoz
Supervisor abroad: Carl Ronald Kahn
Home Institution: Faculdade de Ciências Aplicadas (FCA). Universidade Estadual de Campinas (UNICAMP). Limeira , SP, Brazil
Research place: Harvard University, Boston, United States  
Associated to the scholarship:18/07568-6 - The role of physical exercise on Rock protein pathway, and lipogenic regulation and gluconeogenesis in the liver of aged rats., BP.DR

Abstract

Insulin resistance is the major risk factor for type 2 diabetes (T2D) and metabolic syndrome. This phenotype results from a complex interplay between environmental and genetic factors. Offspring from obese or T2D parents display insulin resistance in the skeletal muscle many years before changes in glucose tolerance and in body weight. Thus, the mechanisms involved with the genetic factors that control the cell-autonomous signaling may contribute to the understanding of insulin resistance, T2D and obesity development in later life. Using transcriptional profile from health and T2D subject, this research project will focus in long non-coding RNAs (lncRNAs) that are changed in response to insulin and have potential role in the pathogenesis of insulin resistance in T2D. Among the lncRNAs, NORAD and MALAT1 were regulated by insulin and also down-regulated in T2D cells. Since recent studies are looking to the metabolic role of lncRNAs, the goal of this research project is characterize the role of NORAD and MALAT1 in the control of metabolic pathways in different cells and tissues with gain and loss of function experiments. The lncRNAs profile will be analyzed in the following conditions: 1) C57BL/6J mice exposed to 16 weeks of High Fat diet (liver, skeletal muscle and adipose); 2) leptin-deficient (ob/ob) mice (liver, skeletal muscle and adipose); 3) mice under fast and refed state (liver, skeletal muscle and adipose); 4) lncRNAs profile in myoblast, adipocyte and hepatocyte cell models in response to insulin, fatty acids and glucose levels; 5) lncRNAs NORAD and MALAT1 knockdown and overexpression consequences in metabolic pathways in different cell types. These experiments will be focused in molecular and functional analysis, providing a strong body of scientific evidence about the role of candidate lncRNAs in the regulation of metabolism in obesity, insulin resistance and T2D conditions. (AU)

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