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NMI Regulates Adipose Adaptive Thermogenesis Through TLR4/IRF3 Signaling to Promote Obesity

Ting-Ting Li1,2, Xin-Yuan Zhao3,4,5, Min Zhang1,2

  • 1Zhongshan School of Medicine, Sun Yat-sen University Shenzhen Campus, Sun Yat-sen University, Shenzhen, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|June 2, 2026
PubMed

Insights

Researchers discovered N-Myc and STAT interactor (NMI) as a key factor in obesity. This stress-responsive adipokine suppresses energy expenditure, worsening metabolic dysfunction, but can be targeted for therapeutic benefit.

Area of Science:

  • Metabolic disease research
  • Adipose tissue biology
  • Inflammation and immunity

Background:

  • Obesity-associated inflammation involves damage-associated molecular patterns (DAMPs).
  • The direct role of DAMPs in suppressing energy expenditure and exacerbating metabolic dysfunction is not fully understood.

Purpose of the Study:

  • To identify novel adipokines involved in regulating energy expenditure.
  • To elucidate the mechanisms by which inflammatory cues impact metabolic rate.
  • To explore therapeutic targets for obesity and related metabolic disorders.

Main Methods:

  • Investigated N-Myc and STAT interactor (NMI) as a stress-responsive adipokine.
  • Utilized genetic ablation of Nmi in mouse models of diet-induced obesity (DIO).
  • Analyzed NMI's effects on thermogenesis, adipose tissue browning, and inflammatory signaling pathways (TLR4/IRF3).
  • Assessed therapeutic potential using a monoclonal antibody against NMI.

Main Results:

  • NMI expression and secretion increase in adipocytes under dietary stress and inflammation.
  • Genetic deletion of Nmi protects against DIO by enhancing energy expenditure and cold tolerance.
  • NMI activates TLR4/IRF3 signaling, repressing key thermogenic regulators (PPARα, PGC-1α, UCP1).
  • NMI neutralization ameliorates obesity and reduces adipose tissue inflammation in DIO mice.

Conclusions:

  • NMI is a stress-responsive adipokine that suppresses adaptive thermogenesis.
  • NMI links inflammatory signaling to reduced energy expenditure, contributing to metabolic dysfunction.
  • Targeting NMI offers a potential therapeutic strategy for obesity and metabolic disorders.
Keywords:
IRF3N‐Myc and STAT interactor (NMI)PPARadaptive thermogenesisimmunometabolism

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