Obese subjects often present a low-grade chronic inflammation in the white adipose tissue, which seems to play an important role in the initiation and development of obesity-related diseases. It has been reported that this inflammatory process may be due to a hypoxic state occuring within this tissue. Oxygen is used in current medicine as a treatment for several conditions. The aim of this study is to analyze the effects of 95% O-2 on specific metabolic variables and on the expression of some genes on murine adipocytes. 3T3-L1 adipocytes were exposed during 48 h to different treatments: 95% O-2 hyperoxia (HPx group), CoCl2 (CoCl2 group), hyperoxia with CoCl2 (HPx+CoCl2 group) and 1% O-2 hypoxia (Hx group). Cell viability, intracellular ROS content, glucose utilization, lactate and glycerol concentrations were measured. Also, mRNA expression of HIF-1 alpha, GLUT-1, ANGPTL4, PPAR-gamma, adiponectin, IL-6 and MCP-1 genes was analyzed. Importantly, 95% O-2 decreased cell viability and increased intracellular ROS production. Also, glycerol and lactate release were significantly increased and decreased, respectively, in HPx treated cells. This treatment also provoked a down-regulation of GLUT-1 and ANGPTL-4, while IL-6 and MCP-1 were up-regulated. Exposure to a hyperoxia of 95% 02 provoked an inflammatory response in adipocytes. The two hypoxia-inducing conditions (CoCl2 and 1% O-2) produced different outcomes in metabolic measurements as well as in the expression of some genes (GLUT-1, ANPGTL4, PPAR-gamma and adiponectin), while it remained similar in others (HIF-1 alpha, IL-6 and MCP-1). Indeed, hyperoxia increased significantly the ROS levels and the lipolytic activity, while it reduced lactate production. In addition to the effects on inflammation, the changes in GLUT-1, ANGPTL4 and PPAR-gamma genes lead to suppose that hyperoxia may be beneficial for the hypertrophied adipose tissues of obese subjects and for improving insulin sensitivity.