C109-06 Il-10 Levels in Tissues From Obstructive Sleep Apnea Patients Are Associated With Impaired Insulin Signaling

Introduction Obstructive sleep apnea (OSA) promotes cardiometabolic disease through chronic, low-grade inflammation. Although circulating interleukin-10 (IL-10) levels are inconsistently affected in OSA, we hypothesized that tissue-level anti-inflammatory capacity is depressed in OSA, sustaining systemic inflammation and metabolic dysfunction. To address this gap, we determined whether IL-10 is reduced in human OSA tissues despite inconclusive plasma findings and tested whether exogenous IL-10 can directly restore insulin signaling in human adipose cells, supporting a translational anti-inflammatory strategy. Methods We partnered with the MU OneHealth Biorepository to obtain adipose and colon tissues from adults with OSA and non-OSA controls. Tissues were homogenized and IL-10 concentrations quantified using a high-sensitivity ELISA (Human IL-10 Quantikine HS, R&D HS100C). Freshly obtained OSA adipose tissues were processed to isolate the stromal vascular fraction (SVF). Purified SVF was pre-treated with recombinant human IL-10 (10 ng/mL, 4 h) or vehicle, and then applied to matched donor adipocytes ± exogenous insulin. Insulin pathway activation was assessed by p-Akt (Ser473) immunoblots and normalized to total Akt immunoreactivity. Results IL-10 was significantly reduced in OSA adipose tissues (∼35% lower; 1.25 ± 0.05 vs 1.93 ± 0.78 pg/mg; p≈0.04; n = 5-6) and showed a marked reduction in OSA colon (∼58% lower; 3.86 ± 1.8 vs 9.24 ± 4.58 pg/mg; p = 0.057; n = 5) compared with non-OSA controls. In preliminary functional assays using two independent OSA adipose samples, IL-10-conditioned SVF increased adipocyte insulin signaling versus vehicle, with p-Akt/Akt ratios of 1.54 ± 0.22 vs 1.07 ± 0.21, respectively, after insulin stimulation, indicating partial restoration of insulin pathway responsiveness. Conclusions Tissue IL-10 is reduced in OSA adipose and colonic tissues, consistent with a localized anti-inflammatory deficit that may contribute to cardiometabolic risk. Exogenous IL-10 enhances insulin signaling in primary human adipose preparations from OSA donors, supporting IL-10-based or IL-10-inducing strategies as adjuvants to CPAP to mitigate OSA-related metabolic dysfunction. Supported by NIH grant HL166617 This abstract is funded by: NIH grant R01-HL166617