Overview
- University of Pittsburgh researchers report that SerpinB2 supports survival of tissue‑resident macrophages in visceral fat, which suppress inflammation linked to insulin resistance.
- In obesity, SerpinB2 levels fall and resident macrophages decline, increasing adipose inflammation and worsening insulin response in mouse models and human fat samples.
- Selective depletion of these resident macrophages aggravated glucose intolerance in obese mice, while protecting them improved metabolic outcomes.
- Antioxidant supplementation in insulin‑resistant mice boosted resident macrophage levels and improved insulin sensitivity, reinforcing the proposed mechanism.
- The team is pursuing a small molecule to raise SerpinB2 for human trials, framing the approach as a potential complement or alternative to GLP‑1 drugs pending clinical evidence.