Diabetes is a collection of conditions that result in too much glucose (sugar) in the blood. Type 1 Diabetes is an autoimmune disease in which the pancreas produces little to no insulin due to an overactive immune system attacking the insulin producing cells in the pancreas. Insulin is a hormone that regulates the metabolism of fats, carbohydrates and protein by controlling the absorption of glucose from the blood into other areas of the body. Patients with Type 1 Diabetes have to take supplemental insulin to keep their glucose levels regulated. Type 2 Diabetes has recently been gaining ground to be classified as an autoimmune disease. A patient with Type 2 produces enough insulin, however, their cells don’t react properly to it creating a condition called insulin resistance. The pancreas continues to create an overabundance of insulin in an attempt to feed the cells. The level of sugar in the blood increases to dangerous levels resulting in the symptoms associated with Type 2 Diabetes.
Patients with diabetes often experience damage to nerves causing neuropathy. Over time, high levels of blood sugar may damage the blood vessels resulting in a loss of circulation to limbs. This is why some patients experience ulcers that don’t heal and potentially require amputation.
Hyperbaric oxygen therapy has been utilized in the treatment of diabetes for a variety of reasons. It has been proven that extensive treatments can produce new blood vessels, a process called angiogenesis. By creating new routes for blood to flow through, the patient can experience better circulation, especially to limbs that have been affected by diabetic induced tissue damage. Many patients have reported a reduction or complete cessation of neuropathy. Increased circulation may also prevent the need for limb removal in patients with severe diabetic ulcers. Hyperbarics has been extensively studied for its healing potential of slow or non-healing wounds, especially in diabetes. Hyperbarics has also been shown to regulate glucose levels which may help control insulin production.
The carotid bodies (CBs) are peripheral chemoreceptors that respond to hypoxia increasing minute ventilation and activating the sympathetic nervous system. Besides its role in ventilation we recently described that CB regulate peripheral insulin sensitivity. Knowing that the CB is functionally blocked by hyperoxia and that hyperbaric oxygen therapy (HBOT) improves fasting blood glucose in diabetes patients, we have investigated the effect of HBOT on glucose tolerance in type 2 diabetes patients. Volunteers with indication for HBOT were recruited at the Subaquatic and Hyperbaric Medicine Center of Portuguese Navy and divided into two groups: type 2 diabetes patients and controls. Groups were submitted to 20 sessions of HBOT. OGTT were done before the first and after the last HBOT session. Sixteen diabetic patients and 16 control individual were included. Fasting glycemia was143.5 ± 12.62 mg/dl in diabetic patients and 92.06 ± 2.99 mg/dl in controls. In diabetic patients glycemia post-OGTT was 280.25 ± 22.29 mg/dl before the first HBOT session. After 20 sessions, fasting and 2 h post-OGTT glycemia decreased significantly. In control group HBOT did not modify fasting glycemia and post-OGTT glycemia. Our results showed that HBOT ameliorates glucose tolerance in diabetic patients and suggest that HBOT could be used as a therapeutic intervention for type 2 diabetes.
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The role of hyperbaric oxygen therapy (HBOT) in the treatment of acute ischemic stroke is controversial. This study aims to investigate whether the peripheral insulin sensitivity of type 2 diabetes patients suffering from intracerebral hemorrhage can be increased after HBOT.
Fifty-two type 2 diabetes participants were recruited after being diagnosed with intracerebral hemorrhage in our hospital. Insulin sensitivity was measured by the glucose infusion rate during a hyperinsulinemic euglycemic clamp (80 mU m−2 min−1) at baseline and 10 and 30 days after HBOT sessions. Serum insulin, fasting glucose, and hemoglobin A1C were measured in fasting serum at baseline and after HBOT sessions. In addition, early (∼10 days after onset) and late (1 month after onset) outcomes (National Institutes of Health Stroke Scale, NIHSS scores) and efficacy (changes of NIHSS scores) of HBOT were evaluated.
In response to HBOT, the glucose infusion rate was increased by 37.8%±5.76% at 1 month after onset compared with baseline. Reduced serum insulin, fasting glucose, and hemoglobin A1C were observed after HBOT. Both early and late outcomes of the HBOT group were improved compared with baseline (P<0.001). In the control group, there was significant difference only in the late outcome (P<0.05). In the assessment of efficacy, there were statistically significant differences between the groups when comparing changes in NIHSS scores at 10 days and 1 month after onset (P<0.05).
Peripheral insulin sensitivity was increased following HBOT in type 2 diabetes patients with intracerebral hemorrhage. The HBOT used in this study may be effective for diabetes patients with acute stroke and is a safe and harmless adjunctive treatment.
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In conclusion, in this pilot study involving 25 sub-jects with T2DM, significant benefits were noted with improvements in glycemic control and C-peptide levels and reduction in insulin requirements. If these benefits persist, the long-term complications of diabetes may be avoided, decreasing the morbidity and mortality of the disease.
This phase I clinical trial of ASC in conjunction with HBO in patients with T2DM has resulted in encouraging preliminary results that requires confirmation in a con-trolled, randomized prospective trial.
See study here.
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