Chronic intermittent hypoxia induces liver injury in mice with diet induced obesity via TLR4/MyD88/MAPK/NF-kB signaling pathways

Introduction: Obstructive sleep apnea (OSA) causes chronic intermittent hypoxia (CIH) during sleep. Inflammatory processes and oxidative stress are known to play a key role in the development of metabolic complications induced by CIH. The purpose of this study was to investigate the proteins related to inflammation in liver subjected to CIH with diet-induced obesity (DIO). Methods: Eight-week old male C57BL/6J mice were fed a high fat or regular diet for 12 weeks and then exposed to CIH or room air for 4 weeks. At the end of the exposure, we examined several genes including myeloid differentiation primary response protein 88 (MyD88), Toll/interleukin-1-receptor-domain-containing adaptor-inducing interferon-β (TRIF), I kappa B (I-κB), nuclear factor kappa B (NF-κB), Toll-like receptor 4 (TLR4), p38 MAP kinase (MAPK), JNK and ERK activation in liver tissue. Results: There was a significant reduction in body weight in DIO mice exposed to CIH steadily through 4 weeks compared with DIO group exposed to room air (P Conclusion: Exposure to CIH in DIO mice by simulating OSA patients leads to hepatic inflammation via TLR4/MyD88/MAPK/NF-kB signaling pathways.