The Influence of Physical Exercise on the Expression and Hypothalamic Function of the MFSD2A Receptor

• Grant number: 25/20959-8
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: November 01, 2025
• End date: October 31, 2026
• Field of knowledge: Health Sciences - Nutrition - Nutrition Biochemistry
• Principal Investigator: Dennys Esper Corrêa Cintra
• Grantee: Danillo Henrique Travensolo Buoro
• Host Institution: Faculdade de Ciências Aplicadas (FCA). Universidade Estadual de Campinas (UNICAMP). Limeira , SP, Brazil

Abstract

Obesity is an alarming global epidemic that continues to advance at an unprecedented rate. Due to obesity-induced metabolic disorders, damage to the central nervous system (CNS) has been consistently evidenced by science. Neuroinflammation, followed by neurodegeneration in the obesogenic context, leads to diseases such as Parkinson's and Alzheimer's in later life, but also to early functional damage throughout the brain. In the hypothalamus, neuroinflammation also leads to uncontrolled hunger and thermogenesis. Part of this damage can be attributed to the loss of sensitivity of the blood-brain barrier (BBB), which impairs permeability control and fails to protect the brain from harmful agents. In this sense, the protein MFSD2A (major facilitator superfamily domain-containing 2a) is the main translocator protein of omega-3 fatty acids (¿3) to the CNS, coupled to the BBB, in addition to being part of the physical structure of the barrier itself. Without MFSD2A during embryonic development and early childhood, the brain is malformed due to nutrient deficiency, but ¿3 deficiencies in adulthood could explain some of the neuronal damage observed in obesity. In parallel, physical exercise can positively interfere with the regulation of nutritional receptors, such as GPR120, another cellular receptor for ¿3. Thus, the objective of the project is to evaluate the potential of exercise to induce restoration of the quantity and function of the MFSD2A protein in the hypothalamus of obese mice.If this occurs, the combination of physical exercise and specific nutrients may represent another anti-obesogenic therapeutic strategy to control associated comorbidities. (AU)