Effect of Hyperbaric Oxygen Therapy (HBOT) on Insulin Resistance Associated with Abdominal Obesity in Wistar Rats with Dietary Sucrose-Induced Metabolic Syndrome.

Metabolic syndrome (MS) is a combination of risk factors related to the development of mainly type 2 diabetes mellitus, cardiovascular disease (CVD) and nonalcoholic fatty liver disease (NAFLD). Its prevalence has increased worldwide, and healthcare systems will face major challenges in addressing this problem. The aim of this work was to evaluate the effect of hyperbaric oxygen therapy (HBOT) on insulin resistance (IR) and obesity associated with MS in Wistar rats. The experimental design consisted of three groups of sucrose-induced MS rats: the MS group that consumed sucrose (MS-Suc; n=5), the MS group that ingested sucrose and HBOT (MS-Suc-HBOT; n=5), the MS group that did not consume sucrose and that received HBOT (MS-HBOT; n=5) and the control group. The rats received HBOT for 20 d at 2.4 atmospheres absolute (ATA) for 60 min. Subsequently, the rats were euthanized, and body fat weight, serum biochemical parameters and microscopic analysis of adipose tissue were determined. Rats with hyperoxia had decreased body weight, adipose tissue hypertrophy, and abdominal and epididymal fat. Likewise, markers of insulin resistance (glucose, insulin and HOMA-IR), biochemical parameters of dyslipidemia (cholesterol and triglycerides) and nonalcoholic fatty liver (AST and ALT) decreased; in contrast, compared to the control group, HBOT increased the 1/HOMA-IR, HOMA-ßCell and McAuley indexes, which were related to the improvement in insulin sensitivity (p<0.05; p<0.01). HBOT showed beneficial effects in the treatment of IR and obesity associated with sucrose-induced metabolic syndrome in Wistar rats.

Clinical efficacy of adjuvant therapy with hyperbaric oxygen in diabetic nephropathy.

Background and objective: Diabetic kidney disease (DKD) is the most common microvascular chronic complication of diabetes mellitus. Hyperbaric oxygen (HBO2) therapy will increase the partial pressure of oxygen (PaO2) and may improve cell repair processes, which can lead to better renal function. The objective of this study was to quantify the efficacy of adjuvant HBO2 to increase the glomerular filtration rate and urinary albumin excretion in diabetic patients, as well as determine its effectiveness to modify the clinical course of DKD. Materials and methods: An experimental study was performed on patients with stage 3 and 4 DKD. Twenty sessions of HBO2 or ambient air in a hyperbaric chamber were administered. Estimated glomerular filtration rate, urine albumin:creatinine ratio calculation and clinical stage stratification were made prior to and after HBO2 administration. A descriptive, inferential and clinical efficacy analysis was performed. Results: Urinary albumin/creatinine (UACR) mean values prior to HBO2 were 1452.9 ± 644.3 mg/g and decreased to 876.1 ± 504.0 mg/g at the end of the study (p=0.06). The patients in the control group showed a UACR mean of 2784.5 ± 2128.6 mg/g and 2861.4 ± 2424.2 mg/g at baseline and at the end of the study, respectively (p=0.82). Patients in the experimental/HBO2 group showed an estimated GFR of 27.3 ± 9.5 mL/min /1.73m2 before HBO2, with a 34.4 ± 6.9 mL/min/1.73m2 after treatment (p=0.017); control group eGFR was 30.1 ± 9.2 mL/min/1.73m2, decreasing to 22.2 ± 6.8 mL/min/1.73m2 (p=0.004). Relative risk 0.00, relative risk reduction -100%, absolute risk reduction -71.4%, 95% CI (-104.9% to -38.0%), NNT 1, 95% CI (1 to 3). Conclusions: Management with HBO2 for DKD was associated with decreased excretion urinary albumin, improved GFR and clinical stage of patients in stages 3 and 4 of kidney damage unlike those receiving ambient air..