Assessment of insulin sensitivity during hyperbaric oxygen treatment.
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ABSTRACT: Introduction
Previous studies using a hyperinsulinaemic, euglycaemic glucose clamp have demonstrated an increase in peripheral insulin sensitivity in men with and without Type-2 diabetes mellitus on the third and thirtieth hyperbaric oxygen treatment (HBOT) session. In two studies using different techniques for assessment of insulin sensitivity, we investigated the onset and duration of this insulin-sensitising effect of HBOT.Methods
Men who were obese or overweight but without diabetes were recruited. One study performed a hyperinsulinaemic euglycaemic glucose clamp (80 mU.m-2.min-1) at baseline and during the first HBOT exposure (n = 9) at a pressure of 203 kPa. Data were analysed by paired t-test. The other study assessed insulin sensitivity by a frequently sampled intravenous glucose tolerance test (FSIGT) at three time points: baseline, during the third HBOT and 24-hours post-HBOT (n = 9). Results were analysed by repeated-measures ANOVA.Results
There was a significant 23% increase in insulin sensitivity by clamp measured during the first HBOT exposure. The FSIGT showed no significant changes in insulin sensitivity.Conclusions
The hyperinsulinaemic, euglycaemic glucose clamp demonstrated a significant increase in peripheral insulin sensitivity during a single, 2-hour HBOT session in a group of men who were obese or overweight but without diabetes. As an alternate technique for assessing insulin sensitivity during HBOT, the FSIGT failed to show any changes during the third HBOT and 24-hours later, however modification of the study protocol should be considered.
SUBMITTER: Wilkinson D
PROVIDER: S-EPMC7819732 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:IntroductionWe have previously shown that hyperbaric oxygen treatment (HBOT) increased insulin sensitivity in men who were obese or overweight, both with and without type 2 diabetes. The aim of this study was to test whether this insulin-sensitising effect is seen in hyperbaric air (HA).MethodsMen with type 2 diabetes who were obese or overweight were randomised to two groups: HBOT (n = 13) or HA (n = 11). A hyperinsulinaemic euglycaemic glucose clamp (80 mU·m-2·min-1) was performed at baseline and during hyperbaric intervention. Both groups were compressed to 203 kPa (two atmospheres absolute) for 90 minutes followed by a linear 30-minute decompression. The HBOT group breathed oxygen via a hood while the HA group breathed chamber air. Insulin sensitivity was assessed from the glucose infusion rate (GIR) during the last 30 minutes in the hyperbaric chamber (SS1) and the first 30 minutes after exit (SS2). Data were analysed for within-group effect by paired student t-test and between-group effect by one-way ANOVA.ResultsHBOT increased GIR by a mean 26% at SS1 (P = 0.04) and 23% at SS2 (P = 0.018). There was no significant change in GIR during or after HA. A between-group effect was evident for the change in GIR at SS1 in HBOT vs HA (P = 0.036).ConclusionsThe pathway by which insulin sensitivity is increased in men with type 2 diabetes requires the high oxygen partial pressures of HBOT and should be further investigated. Insulin sensitivity was not changed in hyperbaric air.
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Project description:Aims/hypothesisHyperbaric oxygen (HBO) therapy may improve hyperglycaemia in humans with type 2 diabetes, but underlying mechanisms are unclear. Our objective was to examine the glucometabolic effects of HBO on whole-body glucose disposal in humans with type 2 diabetes.MethodsIn a randomised placebo-controlled crossover trial located at the German Diabetes Center, 12 male individuals with type 2 diabetes (age 18-75 years, BMI <35 kg/m2, HbA1c 42-75 mmol/mol [6-9%]), randomly allocated by one person, underwent 2-h HBO, once with 100% (240 kPa; HBO) and once with 21% oxygen (240 kPa; control, CON). Insulin sensitivity was assessed by hyperinsulinaemic-euglycaemic clamps with D-[6,6-2H2]glucose, hepatic and skeletal muscle energy metabolism were assessed by 1H/31P-magnetic resonance spectroscopy, while high-resolution respirometry measured skeletal muscle and white adipose tissue (WAT) mitochondrial capacity. All participants and people assessing the outcomes were blinded.ResultsHBO decreased fasting blood glucose by 19% and increased whole-body, hepatic and WAT insulin sensitivity about one-third (p<0.05 vs CON). Upon HBO, hepatic γ-ATP concentrations doubled, mitochondrial respiratory control doubled in skeletal muscle and tripled in WAT (p<0.05 vs CON). HBO increased myocellular insulin-stimulated serine-473/threonine-308 phosphorylation of Akt but decreased basal inhibitory serine-1101 phosphorylation of IRS-1 and endoplasmic reticulum stress (p<0.05 vs CON).Conclusions/interpretationHBO-mediated improvement of insulin sensitivity likely results from decreased endoplasmic reticulum stress and increased mitochondrial capacity, possibly leading to low-dose reactive oxygen species-mediated mitohormesis in humans with type 2 diabetes.Trial registrationClinicalTrials.gov NCT04219215 FUNDING: German Federal Ministry of Health, German Federal Ministry of Education and Research, North-Rhine Westfalia Ministry of Culture and Science, European-Regional-Development-Fund, German-Research-Foundation (DFG), Schmutzler Stiftung.
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Project description:IntroductionTreatment of diabetic foot ulcers is complex and often protracted. Hyperbaric oxygen treatment (HBOT) improves wound healing in diabetic ulcers and serves as an important adjunct to regular diabetic wound care. Endothelial dysfunction plays a central role in diabetes-related vascular complications and may be evaluated by a non-invasive technique called peripheral arterial tonometry which measures a reactive hyperaemia index (RHI). We hypothesized that endothelial function measured by peripheral arterial tonometry is impaired in diabetic foot ulcer patients and that HBOT might improve endothelial function.MethodsEndothelial function was prospectively assessed by peripheral arterial tonometry in 22 subjects with diabetic foot ulcers and 17 subjects without diabetes during courses of HBOT. Endothelial function was evaluated before first (baseline) and 30th treatments, and at 90-day follow-up. Serum insulin growth factor-I (IGF-I) concentrations were determined by immunoassay. Results were compared to 23 healthy subjects.ResultsNo baseline differences were found in endothelial function between subjects with diabetes, HBOT patients without-diabetes and healthy control subjects (RHI; 1.26, 1.61 and 1.81, respectively). No significant changes in RHI were found in patients with (P = 0.17) or without (P = 0.30) diabetes during courses of HBOT. At 90-day follow-up IGF-I was significantly reduced in the subjects with diabetes (P = 0.001) and unchanged in the group without diabetes (P = 0.99).ConclusionsWe found no significant differences in RHI between subjects with diabetic foot ulcers and patients without diabetes, nor improvement in endothelial function assessed by peripheral arterial tonometry during courses of HBOT.
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Project description:Glioblastoma multiforme (GBM) is the most common type of malignant intracranial tumor in adults. Tumor tissue hypoxia, high mitotic rate, and rapid tumor spread account for its poor prognosis. Hyperbaric oxygen therapy (HBOT) may improve the sensitivity of radio-chemotherapy by increasing oxygen tension within the hypoxic regions of the neoplastic tissue. This review summarizes the research of HBOT applications within the context of experimental and clinical GBM. Limited clinical trials and preclinical studies suggest that radiotherapy immediately after HBOT enhances the effects of radiotherapy in some aspects. HBOT also is able to strengthen the anti-tumor effect of chemotherapy when applied together. Overall, HBOT is well tolerated in the GBM patients and does not significantly increase toxicity. However, HBOT applied by itself as curative strategy against GBM is controversial in preclinical studies and has not been evaluated rigorously in GBM patients. In addition to HBOT favorably managing the therapeutic resistance of GBM, future research needs to focus on the multimodal or cocktail approaches to treatment, as well as molecular strategies targeting GBM stem cells.
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