title: Hyperbaric oxygen therapy increases insulin sensitivity in overweight men with and without type 2 diabetes.
abstract: OBJECTIVE
  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.
authors.affiliation: Discipline of Medicine, The University of Adelaide, Hyperbaric Medicine Unit, Royal Adelaide Hospital North Terrace, Adelaide, South Australia 5000, Australia, Phone: +61-(0)8-8222-5116, Fax: +61-(0)8-8232-4207, E-mail: david.wilkinson@health.sa.gov.au.
authors.forename: David
authors.initials: D
authors.lastname: Wilkinson
authors.affiliation: Hyperbaric Medicine Unit, Royal Adelaide Hospital, Adelaide, Australia.
authors.forename: Mirjam
authors.initials: M
authors.lastname: Nolting
authors.affiliation: Discipline of Medicine, The University of Adelaide, Adelaide, Australia.
authors.forename: Mohd Kaisan
authors.initials: MK
authors.lastname: Mahadi
authors.affiliation: Discipline of Medicine, The University of Adelaide, Adelaide, Australia.
authors.forename: Ian
authors.initials: I
authors.lastname: Chapman
authors.affiliation: Discipline of Medicine, The University of Adelaide, Adelaide, Australia.
authors.forename: Leonie
authors.initials: L
authors.lastname: Heilbronn
mesh_terms: D000273:Adipose Tissue / Q000737:chemistry; D001786:Blood Glucose / Q000032:analysis; D018932:Chemokine CCL2 / Q000032:analysis; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000378:metabolism*; D005215:Fasting / Q000097:blood; D005947:Glucose / Q000008:administration & dosage; D006801:Humans; D006931:Hyperbaric Oxygenation; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D015850:Interleukin-6 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000378:metabolism; D050177:Overweight / Q000097:blood / Q000378:metabolism*; D053573:Receptors, Interleukin-1 Type I / Q000037:antagonists & inhibitors; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D001786:Blood Glucose; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D007328:Insulin; D015850:Interleukin-6; D053573:Receptors, Interleukin-1 Type I; D014409:Tumor Necrosis Factor-alpha; D005947:Glucose
keywords: Endocrinology; diabetes; hyperbaric oxygen; hyperbaric research; inflammation; metabolism; obesity