Study of changes in endocrine capacities in different anatomical adipose tissues induced by chronic iatrogenic hypercortisolism

• Grant number: 19/06805-7
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: May 01, 2019
• End date: April 30, 2021
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Fabio Bessa Lima
• Grantee: Maria Clara Soares Casagrande
• Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated research grant: 16/25129-4 - Iatrogenic Chronic Hypercortisolism and its implications to the adipose tissue plasticity an analysis of the dynamics of adipose tissue distribution in an experimental model of Cushing's Syndrome, AP.TEM

Abstract

For a long time, adipose tissue was seen only as a metabolic support, to which a merely passive functional role was attributed. However, in recent years, the discovery of the ability to secrete numerous biologically active compounds has caused this tissue to gain the status of an endocrine organ, and the compounds that are only produced and secreted by it, are called adipokines. Among these, adiponectin and leptin are well known, mainly, for their physiological functions. Both are involved in the regulation of adiposity and, therefore, the imbalance in the synthesis and secretion of these are related to numerous metabolic disorders, from which adipose tissue plays a central role. In view of this, individuals exposed chronically to glucocorticoids in excess show are distribution of adipose mass, in addition to a typical pathological condition, in which each adipose deposit may be influencing differently through an atypical secretory pattern of these adipokines. Thus, the objective of this project is to investigate the endocrine function of different fat pads and, how chronic hypercortisolism interferes with these abilities through culture techniques of primary adipocytes from animals treated chronically with glucocorticoids, gene expression and protein quantification of the secretion of these adipokines. In addition, other parameters will be analyzed in order tounder stand how the secretory pattern of these adipokines influences the pathophysiology of chronic hypercortisolism.