Hyperbaric oxygen therapy (HBOT) has been used to provide oxygen to underperfused organs following ischemia or carbon monoxide intoxication. Various beneficial consequences of HBOT have been reported, including wound healing, anti-inflammatory action, and cell survival; however, the molecular mechanisms underlying these effects have not been elucidated yet. We applied a single HBOT program consisting of administration of 2.8 atmospheres absolute (ATA) for 45 min, followed by 2.0 ATA for 55 min, to 10 male volunteers without any metabolic disease. Within 1 week of HBOT, there was no alteration in serum biochemical variables, except for an increase in triglyceride content. As a mitochondrial stress indicator, the serum concentration of growth differentiation factor 15 was reduced by HBOT. The circulating level of γ-glutamyltransferase was also decreased by HBOT, suggesting an attenuation of oxidative stress. HBOT increased adiponectin and reduced leptin levels in the serum, leading to an elevated adiponectin/leptin ratio. This is the first study to investigate the effect of HBOT on serum levels of metabolic stress-related biomarkers. We suggest that HBOT attenuates mitochondrial and oxidative stresses, and relieves metabolic burdens, indicating its potential for use in therapeutic applications to metabolic diseases.
Keywords: biomarker; hyperbaric oxygen therapy; mitochondria; oxidative stress.