Effects of Nicotinamide Riboside supplementation on mitochondrial function and intestinal permeability of obese mice

• Grant number: 24/22330-7
• Support Opportunities: Scholarships in Brazil - Master
• Start date: August 01, 2025
• End date: July 31, 2027
• Field of knowledge: Health Sciences - Nutrition - Nutrition Biochemistry
• Principal Investigator: Eduardo Rochete Ropelle
• Grantee: Thamires da Silva Santos
• Host Institution: Faculdade de Ciências Aplicadas (FCA). Universidade Estadual de Campinas (UNICAMP). Limeira , SP, Brazil

Abstract

The intestine is an organ that significantly influences the immune response and other systemicresponses. However, several factors can impact its functionality and alter the microbiota composition and intestinal activity. Individuals with obesity have an imbalance of pro-inflammatory and anti-inflammatory bacteria, modifying the content and activity of tightjunction proteins, compromising intestinal integrity, and increasing intestinal permeability. In parallel, obesity compromises the functioning of mitochondria, which are essential for theactivity of intestinal cells. Interestingly, mitochondrial dysfunction in the intestinal epithelium contributes decisively to increased intestinal permeability, making this organelle an important therapeutic target for controlling the intestinal barrier in cases of obesity. Recent studies demonstrate that NAD+ precursors can stimulate mitochondrial repair mechanisms, such asUPRmt, mitochondrial unfolded-protein response, improving the function of the organelle.Over the past 10 years, our group has been dedicated to understanding the effects ofNicotinamide Riboside (NR), a NAD+ precursor derived from vitamin B3, on UPRmt activation and mitochondrial activity in multiple tissues. Given the above, the present project aims to investigate the effects of oral treatment with NR on mitochondrial activity and intestinal permeability in obese mice. The results of this study may contribute to the understanding of the interactions between NAD+ metabolism, mitochondrial repair mechanisms and intestinalpermeability in obesity.