Effect of Hyperbaric Oxygen Therapy on Fatty Acid Composition and Insulin-like Growth Factor Binding Protein 1 in Adult Type 1 Diabetes Mellitus Patients: A Pilot Study

Hyperbaric Oxygen Therapy and Vascular Complications in Diabetes Mellitus

“…94 Hyperbaric oxygen therapy triggers a number of molecular mechanisms in the body that lead to positive therapeutic effects in patients with DM and vascular complications ( Table 1). Numerous studies have shown that HBOT improves systemic hemodynamics and microcirculation, 95,96 accelerates angiogenesis, 97 stimulates the antioxidant protection, 98 increases fibroblast proliferation and collagen synthesis, 99 inhibits inflammation, 100,101 exerts antiatherogenic effects, 102 and reduces the atherosclerotic plaque area. 91 Increase in the pO 2 that remains for 4 to 6 hours after HBOT, provides mitochondrial respiration and cell survival in the state of hypoxia, 103 inhibits apoptosis of the pancreatic b-cells, 100,104 reduces leukocyte adhesion, 105 enhances bactericidal activity of leukocytes, 106 and reduces endothelial dysfunction, 107 thereby contributing to the reduction in inflammation and following vascular complications in patients with DM.…”

“…128 Our results show that HBOT exerts anti-inflammatory and antiatherogenic effects by a mechanism involving changes in plasma FA level and composition by lowering plasma levels of proinflammatory FA and elevating levels of anti-inflammatory and antiatherogenic n-3 polyunsaturated fatty acids (n-3 PUFA) in plasma of patients with DM, especially docosahexaenoic acid. 102 High level of n-3 PUFA in plasma improves insulin sensitivity and decreases hyperglycemia by the mechanism which involves the binding of n-3 PUFA to membrane receptors such as G-protein-coupled receptor 40 (GPR40) in b-cells and GPR120 in adipocytes as well as activation of peroxisome proliferator-activated receptor alpha (PPAR-a) and PPAR-g by n-3 PUFA in the liver. [129][130][131][132] High levels of n-3 PUFA in plasma and erythrocyte membranes have beneficial effects on glucose and lipid metabolism and are associated with a reduced risk of developing IDDM.…”

“…[129][130][131][132] High levels of n-3 PUFA in plasma and erythrocyte membranes have beneficial effects on glucose and lipid metabolism and are associated with a reduced risk of developing IDDM. 102,[133][134][135] The literature data show that HBOT affects the composition and level of FFA in plasma and cell membranes by inhibiting the hypoxia-induced signaling cascade, which disrupts membrane structure, prevents FA release from cell membranes, reduces ROS synthesis and lipid peroxidation, and affects the activity of enzymes involved in elongation and desaturation FFA. 72,136,137 Hyperbaric oxygen therapy also improves dyslipidemia associated with an increased risk of accelerating the process of atherosclerosis and cardiovascular disease in patients with DM and vascular complications, 63,138,139 which was also shown in our prospective pilot study.…”

“…116 We have previously shown that HBOT causes downregulation of iNOS expression and activity via signaling pathways of protein kinase B (Akt), extracellular signal-regulated kinases, and nuclear factor kappa B in patients with DMT2 and thereby exerting anti-inflammatory effects. 101 Also, HBOT decreases the level of inflammatory markers such as cytokines (interleukin 1 and tumor necrosis factor α), 113,105 C-reactive protein, 101,117 free fatty acid (FFA), and NO 101,102 in the blood of patients with DM. In addition, HBOT improves glucose metabolism in patients with DM and vascular complications, most probably by increasing insulin sensitivity 118 –120 via upregulation of peroxisome proliferator-activated receptor gamma (PPAR-γ) expression 121,122 as well as increase in adiponectin level, which further regulates the expression of glucose transporter 4 by Akt and mediate glucose uptake.…”

“…72,136,137 Hyperbaric oxygen therapy also improves dyslipidemia associated with an increased risk of accelerating the process of atherosclerosis and cardiovascular disease in patients with DM and vascular complications, 63,138,139 which was also shown in our prospective pilot study. 102 Teshigawara et al reported that HBOT regulates lipid metabolism in mice with DM, by increasing expression of enzyme involved in β-oxidation of FA in mitochondria-carnitine palmitoyltransferase 1 (CPT-1), as well as expression of PPARα and peroxisome proliferator gamma coactivator-1 α, involved in transcription of CPT-1 and regulation of lipid metabolism. 140 All these data together indicate that HBOT is an effective component of the complex treatment of patients with DM and associated microvascular and macrovascular complications.…”