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Study of the metabolic and functional adaptation of macrophages by different adipocyte populations.

Grant number: 25/00279-2
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Start date: April 01, 2025
End date: March 31, 2026
Field of knowledge:Biological Sciences - Immunology
Principal Investigator:Pedro Manoel Mendes de Moraes Vieira
Grantee:Isabela Rebeca Fernandes Sacramento
Host Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
Associated research grant:20/16030-0 - Immunometabolic adaptation of tissue resident macrophages in health and disease, AP.TEM

Abstract

The low-grade chronic inflammation observed in obesity is directly associated with insulin resistance. In visceral adipose tissue, macrophages exhibit different phenotypes. Among these, pro-inflammatory macrophages stand out, contributing to chronic inflammation and insulin resistance in obesity. These macrophages secrete inflammatory cytokines such as TNF, IL-6, and IL-1beta, exacerbating the low-grade systemic inflammatory state induced by obesity. On the other hand, repair/resolution phenotype macrophages maintain tissue homeostasis and are reduced in obesity. In addition to their immunological profile, the energy metabolism of these cells can also vary depending on the tissue in which they reside. Adipocytes also exhibit phenotypic and functional diversity. In white adipose tissue (WAT), three classes of adipocytes have been described, with specific locations and protein markers, including adipokine-leptin (Adipo-LEP), perilipin-1 (PLIN1), perilipin-4 (PLIN4), and serum amyloid proteins A1 (SAA1) and A2 (SAA2). However, it is still unclear how the distinct metabolic and immunological profiles of macrophages are influenced by the identity of adjacent adipocytes. Therefore, it is possible that different adipocyte classes specifically modulate macrophage phenotype and function. Our objective is to determine how different adipocyte populations modulate the phenotype, function, and metabolism of macrophages.

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