Objective To provide an comprehensive evaluation of the correlation between sleep apnea hypopnea syn?drome (SAHS) and nonalcoholic fatty liver disease (NAFLD). Methods The various case-control studies on the relation?ship between SAHS and NAFLD were retrieved from all kinds of large-scale databases at home and abroad (including Web of science, EMbase, Pubmed, Springer Link, EBSCO Databases, CNKI, CQVIP, Wanfang Data). The quality evaluation of in?cluded studies was made by two independent researchers. RevMan 5.1 and stata 12.0 software were used for meta-analysis. Results A total of 11 qualified documents were included in this study. Meta analysis showed that the relative risk of NAFLD was increased in SAHS patients than non-SAHS patients (RR=2.82, 95%CI:2.03-3.92, P<0.01). The serum ala?nine aminotransferase (ALT) increased in SAHS patients (SMD=0.53, 95% CI:0.02-1.05, P < 0.05). Compared with non-SAHS patients, the apnea-hypopnea index (AHI) was significantly higher in SAHS patients combined with severe NAFLD than those combined with mild NAFLD (SMD=1.42, 95%CI:0.12-2.72, P < 0.05). Conclusion The risk of NAFLD in?creases in SAHS patients. The severity of NAFLD is relatively higher with the severity of intermittent hypoxia.

Background and Aim:Sulfotransferase(SULT)-mediated sulfation and steroid sulfatase(STS)-mediated desulfation represent two critical mechanisms that regulate the chemical and functional homeostasis of endogenous and exogenous molecules.STS catalyzes the hydrolysis of steroid sulfates to form hydrox-ysteroids.Oxygenated cholesterol derivative oxysterols are known to be endogenous ligands of the liver X receptor(LXR),a nuclear receptor with anti-cholestasis activity,whereas the sulfated oxysterols antagonize LXR signaling.The conversion of sulfated oxysterols to their non-sulfated counterparts is catalyzed by STS.The aim of this study is to determine whether STS can alleviate cholestasis by increasing the activity of LXR. Methods:Liver-specific STS transgenic mice were created and subject to the lithocholic acid(LCA)-induced model of cholestasis. Results:Transgenic overexpression of STS in the liver promoted bile acid elimination and alleviated LCA-induced cholestasis.The protective effect of the STS transgene was associated with the activation of LXR and induction of LXR target genes,likely because of the increased conversion of the antagonistic oxy-sterol sulfates to the agonistic oxysterols. Conclusions:STS has a novel function in controlling the homeostasis of bile acids by regulating endog-enous LXR ligands.