Disrupting the adiposopathy-inflammation loop: a translational immunometabolic framework for inflammatory disease

Area of Science:

• Immunometabolism
• Adipose tissue biology
• Chronic inflammatory diseases

Background:

• Adipose tissue dysfunction (adiposopathy) is a key factor in chronic inflammation, especially in obesity.
• It involves metabolic and immune alterations, including adipokine dysregulation and macrophage infiltration.
• This dysfunction contributes to an immunometabolic phenotype, linking metabolic health and immune activation.

Purpose of the Study:

• To explore adiposopathy as a measurable immunometabolic state influencing inflammatory disease.
• To investigate the potential of targeting adipose tissue dysfunction for therapeutic benefit.
• To examine the role of incretin-based therapies in modulating inflammation beyond weight loss.

Main Methods:

• Review of current literature on adiposopathy and its link to inflammation.
• Analysis of the TOGETHER-PsA trial data on tirzepatide and IL-17 inhibition in psoriatic arthritis.
• Examination of experimental evidence for GLP-1 and GIP receptor signaling in immune cells.

Main Results:

• Adiposopathy may amplify inflammatory signaling and affect therapeutic response in immune-mediated diseases.
• The TOGETHER-PsA trial showed improved psoriatic arthritis control with tirzepatide plus IL-17 inhibition in overweight/obese patients.
• Emerging evidence suggests incretin-based therapies may have direct anti-inflammatory effects.

Conclusions:

• Adiposopathy represents a therapeutically actionable target in chronic inflammatory diseases.
• Targeting adipose tissue dysfunction could complement existing immune-targeted therapies.
• Further research is needed to elucidate the mechanisms and clinical utility of modulating adiposopathy.