Upregulation of peripheral blood mononuclear cells resistin gene expression in severe obstructive sleep apnea and obstructive sleep apnea with coexisting type 2 diabetes mellitus

Purpose Obstructive sleep apnea (OSA) is characterised by increased systemic inflammation, and is often accompanied with type 2 diabetes mellitus (T2DM) and cardiovascular disease. The aim of this investigation was to evaluate gene expression of resistin, its receptor CAP1 and CD36 as the indicators of the inflammatory changes in PBMCs in relation to the severity of OSA, and the presence of type 2 diabetes mellitus (T2DM) in OSA. Methods Severity of OSA was defined by the apnea/hypopnea index (AHI): AHI < 30: mild to moderate OSA (MM-OSA), AHI ≥ 30: severe OSA (S-OSA). Presence of T2DM was captured: OSA with T2DM (OSA + T2DM), OSA without T2DM (OSA-T2DM). PBMC resistin, CAP1, and CD36 mRNA were determined by real-time PCR. Results Resistin mRNA was significantly upregulated in S-OSA ( N = 54) compared to the MM-OSA ( N = 52, P = 0.043); CAP1 and CD36 mRNA levels did not differ between the groups ( P = 0.302; P = 0.166, respectively). Resistin mRNA was significantly upregulated in OSA + T2DM ( N = 29) compared to the OSA-T2DM ( N = 77, P = 0.029); CAP1 and CD36 mRNA levels did not differ between the groups ( P = 0.662; P = 0.108, respectively). AHI and T2DM were independent predictors of resistin mRNA above the 75th percentile (OR = 3.717 [1.152–11.991]; OR = 3.261 [1.000–10.630], P = 0.042 respectively). Conclusion Resistin gene upregulation in S-OSA indicates its possible contribution to increased inflammation in S-OSA and makes it a possible marker of the disease severity. Resistin gene upregulation in OSA + T2DM suggests that a joint effect of these two comorbidities may have a major contribution to increased inflammation and complications that arise from this state.