Compared to fold change expression of other genes, a small but significant regulation of WDR73 gene expression data. This may be due to different oligonucleotides used for PCR, which are specific for exon 2 and 4, and those for microarray analysis, detecting alternative splicing products. However nothing is known about possible alternative splicing mechanisms of WDR73 RNA. Interestingly, we did not detect a binding site for hypoxiainducible factors 1 and 2 according to our cut off settings. Both findings argue against a role of WDR73 during hypoxia. However we do not rule out that there are further hypoxia responsible elements for those factors, as we also did not detect the HREs described by Garayoa et al. in ADM according to our settings. Therefore future studies may clarify the regulation and function of WDR73. Furthermore we could not only show that most genes, upregulated by hypoxia, harbour binding sites for HIF1A and EPAS1, but also that EPAS1 is upregulated after 16h of hypoxia, indicating a positive feedback mechanism. Looking for general composite promoter models within these genes we did not detect a striking conformity. However, we revealed binding sites for FOXO4 and the forkhead box superfamily within almost every proximal promoter of the upregulated genes. FOXO transcription factors mediate anti-angiogenic effects and play a central role during oxidative stress. In addition, the transcription regulator FOXO4 is known to downregulate the expression of EPO, VEGFA and HIF1A. In this context, the direct overlap of FOX- and HIF-binding sequences within ANKRD37, DDIT4 and PPP1R3C may suggest an interaction or a competition of these factors for binding to the respective promoter elements. We suppose that the FOX-family of transcription factors may play an important role for gene regulation during hypoxia in SGBS adipocytes, likely by impeding excessive expression after hypoxic treatment. However, further studies regarding protein expression patterns in adipocytes will be necessary to test this hypothesis. Taken together, we demonstrated that hypoxia has an extensive effect on gene expression of SGBS adipocytes, which responded with the regulation of genes involved in different crucial biological processes. In addition, the identified hypoxia-regulated genes have been in part MK-1775 suggested to be involved in the regulation of obesity, the incidence of type 2 diabetes, and the metabolic syndrome. However, adipose tissue in vivo consists also of other cell types than the investigated adipocytes. Therefore, additional studies using primary cells e.g. derived from lipoaspirates are needed to be performed to elucidate the relation of whole adipose tissue hypoxia and the chronic inflammation observed in obesity. Nevertheless, we have now established a comprehensive gene expression profile for these adipocytes under hypoxia. Pulmonary dysfunction is common in patients with chronic liver disease and may worsen outcomes. The hepatopulmonary syndrome is recognized as one important cause for abnormal oxygenation in cirrhosis that occurs in up to 32% of patients and significantly impairs quality of life and increases mortality.