NMI Regulates Adipose Adaptive Thermogenesis Through TLR4/IRF3 Signaling to Promote Obesity - PubMed
3 hours ago
- #NMI
- #adaptive thermogenesis
- #obesity
- N-Myc and STAT interactor (NMI) is identified as a stress-responsive adipokine that suppresses adaptive thermogenesis in adipose tissue.
- Genetic ablation of Nmi protects mice from diet-induced obesity by enhancing energy expenditure and cold tolerance via increased brown adipose tissue thermogenesis and white adipose tissue browning.
- Mechanistically, adipose-derived NMI activates TLR4/IRF3 signaling, which transcriptionally represses key thermogenic regulators PPARα, PGC-1α, and UCP1.
- Therapeutically, neutralization of NMI with a monoclonal antibody ameliorates obesity and reduces adipose tissue macrophage infiltration in diet-induced obese mice.
- The study highlights NMI's role in linking inflammatory signaling to suppressed energy expenditure, presenting it as a therapeutic target for obesity and metabolic disorders.