The mystery of UCP1 negative adipocytes present in brown and beige adipose tissues of cold-acclimated mice

• Grant number: 24/16709-3
• Support Opportunities: Scholarships abroad - Research Internship - Scientific Initiation
• Start date: December 01, 2024
• End date: February 28, 2025
• Field of knowledge: Biological Sciences - Pharmacology - Biochemical and Molecular Pharmacology
• Principal Investigator: Patrícia Reckziegel
• Grantee: Giovanna Freitas Rodrigues Jardim
• Supervisor: Jan Jacob Martin Nedergaard-Hansen
• Host Institution: Faculdade de Ciências Farmacêuticas (FCF). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Institution abroad: Stockholm University, Sweden
• Associated to the scholarship: 23/02579-8 - Can peptides derived from the UCP1 protein modulate parameters related to thermogenesis in white and brown adipocytes?, BP.IC

Abstract

Brown adipose tissue (BAT) is well-known as the primary site for non-shivering thermogenesis, a process largely attributed to the high levels of mitochondrial uncoupling protein 1 (UCP1), which serves as a key marker of BAT. Interestingly, UCP1 can also be induced in white adipose tissue (WAT) following a browning event. Recent observations by our group and others have identified adipocytes in interscapular BAT (IBAT) and inguinal WAT (ingWAT) of cold-acclimated mice that exhibit little (UCP1low) or no UCP1 expression (UCP1neg). The aim of this project is to investigate these UCP1low and UCP1neg adipocytes and characterize the expression of proteins associated with possible UCP1-independent thermogenic pathways within these specific adipocyte populations. We will analyze IBAT and ingWAT from wild-type and UCP1-knockout (UCP1-KO) mice that have been exposed to cold conditions (4°C) for at least one month. Using immunohistochemistry, we will assess the presence of UCP1, and of ATP synthase, respiratory chain proteins, and other proteins involved in possible alternative thermogenic pathways (e.g., creatine kinase B [CKB], glycerol kinase [GK], etc.). Through this research, we aim to reveal whether UCP1-independent thermogenic mechanisms may exist in adipocytes with significant phosphorylation capacity, particularly in those lacking UCP1.