J Inflamm Res. 2026 Aug 5;19:590431. doi: 10.2147/JIR.S590431. eCollection 2026.
ABSTRACT
BACKGROUND: Macrophage-driven inflammation in adipose tissue contributes to chronic intermittent hypoxia (CIH)-induced metabolic disorders, but the underlying mechanisms remain unclear. Adiponectin (Ad), an abundant adipokine secreted by adipocytes, plays a crucial role in insulin sensitivity. We tested the hypothesis that CIH-induced macrophage inflammation requires adipocyte-derived paracrine signals and that Ad attenuates this process.
METHODS: Using a co-culture approach, we investigated the roles of adipocytes and Ad in CIH-induced macrophage inflammation. Direct co-culture involved physical interaction between iBMDM macrophages and 3T3-L1 adipocytes, while indirect co-culture used adipocyte-conditioned media. After CIH and Ad treatment, inflammatory factor levels in conditioned media were quantified. Statistical significance was set at P < 0.05.
RESULTS: CIH did not directly trigger inflammatory factor release from individually cultured iBMDM cells or 3T3-L1 adipocytes. However, CIH significantly increased inflammatory factor release in co-cultured cells. Ad alleviated the pro-inflammatory effect of adipocytes on macrophages under CIH conditions.
CONCLUSION: CIH disrupts adipocyte function and promotes macrophage inflammation via paracrine mechanisms.
PMID:42572695 | PMC:PMC13453351 | DOI:10.2147/JIR.S590431
