Effects of Hyperoxia on Oxygen-Related Inflammation with a Focus on Obesity

Abstract

Several studies have shown a pathological oxygenation (hypoxia/hyperoxia) on the adipose tissue in obese subjects. Additionally, the excess of body weight is often accompanied by a state of chronic low-degree inflammation. The inflammation phenomenon is a complex biological response mounted by tissues to combat injurious stimuli in order to maintain cell homeostasis. Furthermore, it is believed that the abnormal oxygen partial pressure occurring in adipose tissue is involved in triggering inflammatory processes. In this context, oxygen is used in modern medicine as a treatment for several diseases with inflammatory components. Thus, hyperbaric oxygenation has demonstrated beneficial effects, apart from improving local tissue oxygenation, on promoting angiogenesis, wound healing, providing neuroprotection, facilitating glucose uptake, appetite, and others. Nevertheless, an excessive hyperoxia exposure can lead to deleterious effects such as oxidative stress, pulmonary edema, and maybe inflammation. Interestingly, some of these favorable outcomes occur under high and low oxygen concentrations. Hereby, we review a potential therapeutic approach to the management of obesity as well as the oxygen-related inflammation accompanying expanded adipose tissue, based on elevated oxygen concentrations. To conclude, we highlight at the end of this review some areas that need further clarification.

Figure 1

Effects of obesity on adipose tissue. Oxidative stress, altered PO₂, and endoplasmic reticulum stress are potential triggering factors for metaflammation development. This chronic low-grade inflammation is associated with proinflammatory adipokines release and the concomitant macrophages migration to metaflammation zone. And, then, positive feedback for proinflammatory signals is perpetuated in the tissue which could be related to posterior metabolic disorders. IL-1β: Interleukin-1β; IL-6: Interleukin-6; TNF-α: tumor necrosis factor-α; LEP: leptin; MS: metabolic syndrome; CVD: cardiovascular disease; IR: insulin resistance.

Figure 2

Effects of hypoxia on the secretion of key proteins in mice and human adipocytes and in adipose tissue of C57BL/6J mice (green up arrow) increased and (red down arrow) decreased protein in response to hypoxia). ADIPOQ: adiponectin; ANGPTL4: Angiopoietin-like protein 4; APLN: Apelin; DPP4: dipeptidyl peptidase-4; GLUT-1: Glucose Transporter 1; HIF-1α: hypoxia-inducible factor-1α; IL-6: Interleukin-6; IL-10: Interleukin-10; LEP: leptin; MIF: macrophage migration inhibitory factor; MCP-1: monocyte chemoattractant protein-1; PAI-1: plasminogen activator inhibitor-1; VEGF: vascular endothelial growth factor; TNF-α: tumor necrosis factor-α.