Aims: The onset of insulin resistance is an important metabolic event in the development of type 2 diabetes. For patients with type 2 diabetes, we recently showed that peripheral insulin sensitivity was increased during hyperbaric oxygen treatment (HBOT). This study aims to investigate whether this occurs in a non-patient population with and without type 2 diabetes, along with the mechanism of this effect.
Methods: Overweight and obese male participants were recruited from the community, 11 without and eight with type 2 diabetes. Insulin sensitivity was measured by the glucose infusion rate (GIR) during a hyperinsulinaemic euglycaemic clamp (80 mU·m⁻²·min⁻¹) at baseline and during the third HBOT session. Monocyte chemo-attractant protein-1 (MCP-1), tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were measured in fasting serum and adipose tissue samples taken for their gene expression at baseline and immediately following four HBOT sessions. Additional fasting serum samples were collected during the first HBOT at 0, 60 and 120 minutes, and 24-hours after the last HBOT.
Results: In response to HBOT, GIR was increased by 29±32% in those without (n=10, P=0.01), and by 57±66% in those with type 2 diabetes (n=7, P=0.04). This increase was maintained for 30 minutes post HBOT. Reduced MCP-1 and TNF-α were observed after HBOT, whereas IL-6 was increased only in individuals without diabetes and this correlated with the increase in insulin sensitivity (r²=0.72, P=0.004).
Conclusions: Peripheral insulin sensitivity was increased following HBOT in overweight or obese males with and without type 2 diabetes; this increase was maintained for at least 30 minutes post HBOT. Changes in inflammatory cytokines may partly explain this effect.
Keywords: Endocrinology; diabetes; hyperbaric oxygen; hyperbaric research; inflammation; metabolism; obesity.