Hyperbaric oxygen and insulin sensitivity

Abstract

Introduction: Obesity is associated with a chronic low grade inflammatory state and the development of insulin resistance and diabetes, while hyperbaric oxygen therapy (HBOT) has demonstrated anti-inflammatory properties. But it was the observation that people with diabetes were susceptible to a fall in blood glucose levels during HBOT that led to an investigation of insulin sensitivity. Methods: Five human studies were reported in four publications. Four studies used the hyperinsulinaemic euglycaemic glucose clamp and one used a frequently sampled intravenous glucose tolerance test (FSIGT) to investigate insulin sensitivity during HBOT. Studies recruited men who were overweight or obese, with and without diabetes. Blood samples for inflammatory cytokines and adipose tissue biopsies for gene expression were taken to investigate possible mechanisms of action. Results: A total of sixty-two men were investigated by glucose clamp and nine by FSIGT. All four glucose clamp studies showed significant within-group increases in insulin sensitivity following exposure to HBOT. First, in a group of patients with (n=5) and without diabetes (n=5) referred for clinical HBOT, there was a 37% increase during the third HBOT and 41% increase during the thirtieth HBOT. Next, in a group of men who were overweight or obese, we found a 29% increase in men without diabetes (n=11) and 57% increase in those with diabetes (n=8) during the third HBOT. Further, the effect was still measurable in the first 30 minutes after exit from the hyperbaric chamber. Pre and post-HBOT testing found reductions in serum TNF-α and MCP-1 while IL-6 increased. Next, in a group of men who were overweight or obese but without diabetes (n=9), we found a significant 23% increase during the first HBOT intervention. There was a significant increase in serum IL-6 after HBOT but no change in TNF-α or MCP-1. The final glucose clamp study randomised men to either HBOT (n=13) or hyperbaric air (n=11) and found a significant between group difference with a 26% increase in insulin sensitivity during HBOT but no significant change in hyperbaric air. The FSIGT study performed the insulin sensitivity test on men who were overweight or obese and without diabetes (n=9) during the third HBOT and 24-hours later but found no changes from baseline. Conclusions: The glucose clamp technique identified an acute increase in insulin sensitivity during HBOT. The effect could be seen in those without diabetes which suggests it is a physiological response to HBOT. Further research is encouraged into this insulin-sensitising effect of HBOT as it could open new therapeutic pathways for glucose regulation. No change to insulin sensitivity was seen in hyperbaric air; although it was a very modest exposure this may be relevant to people in other hyperbaric environments such as diving. The response of serum inflammatory cytokines to HBOT was inconsistent however two studies that showed increased insulin sensitivity during HBOT together with increased serum IL-6 suggest the origin and role of IL-6 requires further investigation.