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Oxygen And Insulin

A Local Glucose-and Oxygen Concentration-based Insulin Secretion Model For Pancreatic Islets

A Local Glucose-and Oxygen Concentration-based Insulin Secretion Model For Pancreatic Islets

Theoretical Biology and Medical Modelling Buchwald; licensee BioMed Central Ltd.2011 Because insulin is the main regulator of glucose homeostasis, quantitative models describing the dynamics of glucose-induced insulin secretion are of obvious interest. Here, a computational model is introduced that focuses not on organism-level concentrations, but on the quantitative modeling of local, cellular-level glucose-insulin dynamics by incorporating the detailed spatial distribution of the concentrations of interest within isolated avascular pancreatic islets. All nutrient consumption and hormone release rates were assumed to follow Hill-type sigmoid dependences on local concentrations. Insulin secretion rates depend on both the glucose concentration and its time-gradient, resulting in second-and first-phase responses, respectively. Since hypoxia may also be an important limiting factor in avascular islets, oxygen and cell viability considerations were also built in by incorporating and extending our previous islet cell oxygen consumption model. A finite element method (FEM) framework is used to combine reactive rates with mass transport by convection and diffusion as well as fluid-mechanics. The model was calibrated using experimental results from dynamic glucose-stimulated insulin release (GSIR) perifusion studies with isolated islets. Further optimization is still needed, but calculated insulin responses to stepwise increments in the incoming glucose concentration are in good agreement with existing experimental insulin release data characterizing glucose and oxygen dependence. The model makes possible the detailed description of the intraislet spatial distributions of insulin, glucose, and oxygen levels. In agreement with recent observations, modeling also suggests that sm Continue reading >>

Role Of Reactive Oxygen Species In Injury-induced Insulin Resistance

Role Of Reactive Oxygen Species In Injury-induced Insulin Resistance

Acute insulin resistance is common after injury, infection, and critical illness. To investigate the role of reactive oxygen species (ROS) in critical illness diabetes, we measured hepatic ROS, which rapidly increased in mouse liver. Overexpression of superoxide dismutase 2, which decreased mitochondrial ROS levels, protected mice from the development of acute hepatic insulin resistance. Insulin-induced intracellular signaling was dramatically decreased, and cellular stress signaling was rapidly increased after injury, resulting in the hyperglycemia of critical illness diabetes. Insulin-induced intracellular signaling, activation of stress (c-Jun N-terminal kinase) signaling, and glucose metabolism were all normalized by superoxide dismutase 2 overexpression or by pretreatment with antioxidants. Thus, ROS play an important role in the development of acute hepatic insulin resistance and activation of stress signaling after injury. Increased levels of reactive oxygen species (ROS) are correlated with chronic insulin-resistant states, such as type 2 diabetes, obesity, hypertension, cardiovascular disease, and the metabolic syndrome ( 1 5 ). However, recent work indicates that ROS levels may be necessary for normal insulin sensitivity, possibly due to a ROS-mediated decrease in protein tyrosine phosphatase activity ( 6 , 7 ). Little is known about the role of ROS in the acute development of hyperglycemia and insulin resistance in the critical illness diabetes that rapidly develops after surgery, injury, or critical illness. The Leuven study reported that control of hyperglycemia, by intensive insulin therapy in critically ill patients, results in a 3450% reduction in mortality and other morbidities ( 8 ). Since then, achieving euglycemia has become a major therapeutic targ Continue reading >>

Effects Of Oxygen, Insulin, And Glucagon Concentrations On Rat Submandibular Acini In Serum-free Primary Culture

Effects Of Oxygen, Insulin, And Glucagon Concentrations On Rat Submandibular Acini In Serum-free Primary Culture

, Volume 30, Issue12 , pp 833842 | Cite as Effects of oxygen, insulin, and glucagon concentrations on rat submandibular acini in serum-free primary culture The objective of these studies was to develop serum-free culture conditions for dissociated acini from rat submandibular glands. Acini were isolated from the submandibular glands of 4246 d old rats and cultured on reconstituted rat tail collagen containing laminin in 1:1 Hams F12 and Dulbeccos media, supplemented with BSA, transferrin, insulin, T3, EGF, dexamethasone, retinoic acid, carbamylcholine, and trace elements, and gassed with 50% O2. The acini became partly embedded in the collagen gel and rapidly enlarged throughout the first 22 d of culture, maintaining modest seromucous acinar differentiation, as judged morphologically and by mucin secretion. Parallel cultures then were grown under 20, 35, 50, and 65% O2, and evaluated morphologically and by DNA content. Growth and retention of seromucous acinar characteristics were best with 35% O2, but lipid accumulation and cell death were unacceptably high. A spectrum of concentrations of insulin and glucagon then were tried. With 0.05g/ml insulin, cellular growth and organization were orderly, lipid accumulations were not excessive, and moderate differentiation was retained through 15 d of culture. With more than 0.1g/ml insulin added to or subtracted from the optimum, the detrimental effects recurred. Addition of sufficient glucagon counteracted the effects of both optimum and excessive concentrations of insulin. We now have achieved an orderly growth of moderately differentiated rat submandibular acini for 15 d in serum-free primary culture. cell cultureinsulinsalivary glandserum-freesubmandibular gland This is a preview of subscription content, log in to check ac Continue reading >>

How The Keto Diet, Oxygen Therapy, And Insulin Potentiation Therapy Improve Cancer Treatment

How The Keto Diet, Oxygen Therapy, And Insulin Potentiation Therapy Improve Cancer Treatment

The American Cancer Society projects that there will be 1,735,350 new cancer cases and 609,640 cancer deaths in the United States this year. [1] While cancer cases have increased, cancer death rates in the U.S. have been on the decline since the early 1990s meaning, treatments are getting more effective every day. [2] New areas of cancer research around novel therapies like the ketogenic diet, oxygen therapy (HBOT), and insulin potentiation therapy (IPT) offer promising ways to tackle cancer alongside traditional cancer treatments. According to recent Bulletproof Radio ( iTunes ) podcast guest Kris Smith, MD, a top neurosurgeon who specializes in brain tumors at the Barrow Neurological Institute in Phoenix, the downside of some aggressive cancer treatments is that they can cause lifelong side effects in survivors. The challenge is to find effective treatments that arent as damaging to the patient. Were really trying to learn through molecular profiling analysis and a lot of epigenetic changes how to beat cancer, but not beat the patients brain in the process, he says. I really think the ketogenic diet is going to bepart of that magic bullet, the holy grail of treating people with this disease. Ahead, what the science says about these new, less traditional forms of cancer treatment. First, in order to understand how these treatments work, heres a review of how cancer develops in the first place. While there are several different forms of cancer, they are all characterized by uncontrolled cell growth that typically forms a lump or tumor. In the 1920s, German scientist Otto Warburg observed that cancer cells grow at a rapid rate specifically due to glycolysis, the breakdown of glucose or sugar (carbs) into energy. Warburgs hypothesis that cancer cells need a high-carb die Continue reading >>

Reactive Oxygen Species Have A Causal Role In Multiple Forms Of Insulin Resistance

Reactive Oxygen Species Have A Causal Role In Multiple Forms Of Insulin Resistance

Reactive oxygen species have a causal role in multiple forms of insulin resistance Nature volume 440, pages 944948 (13 April 2006) Insulin resistance is a cardinal feature of type 2 diabetes and is characteristic of a wide range of other clinical and experimental settings. Little is known about why insulin resistance occurs in so many contexts. Do the various insults that trigger insulin resistance act through a common mechanism? Or, as has been suggested 1 , do they use distinct cellular pathways? Here we report a genomic analysis of two cellular models of insulin resistance, one induced by treatment with the cytokine tumour-necrosis factor- and the other with the glucocorticoid dexamethasone. Gene expression analysis suggests that reactive oxygen species (ROS) levels are increased in both models, and we confirmed this through measures of cellular redox state. ROS have previously been proposed to be involved in insulin resistance, although evidence for a causal role has been scant. We tested this hypothesis in cell culture using six treatments designed to alter ROS levels, including two small molecules and four transgenes; all ameliorated insulin resistance to varying degrees. One of these treatments was tested in obese, insulin-resistant mice and was shown to improve insulin sensitivity and glucose homeostasis. Together, our findings suggest that increased ROS levels are an important trigger for insulin resistance in numerous settings. Tumor necrosis factor-- and hyperglycemia-induced insulin resistance. Evidence for different mechanisms and different effects on insulin signaling Uysal, K. T., Wiesbrock, S. M., Marino, M. W. & Hotamisligil, G. S. Protection from obesity-induced insulin resistance in mice lacking TNF- function Kusunoki, M., Cooney, G. J., Hara, T. & S Continue reading >>

Repetitive Hyperbaric Oxygen Treatment Increases Insulin Sensitivity In Diabetes Patients With Acute Intracerebral Hemorrhage

Repetitive Hyperbaric Oxygen Treatment Increases Insulin Sensitivity In Diabetes Patients With Acute Intracerebral Hemorrhage

Qian Xu, Yi-ting Wei, Shuang-bo Fan, Liang Wang, Xiao-ping Zhou Department of Brain Surgery, Ningbo Zhenhai Longsai Hospital, Zhejiang, People’s Republic of China Aim: 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. Methods: 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. Results: 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). Conclusion: Peripheral insulin sensitivity was increased following HBOT in type 2 diabetes patients with intracerebral hemorrhage. The HBO Continue reading >>

Protein Tyrosine Phosphatase 1b And Insulin Resistance: Role Of Endoplasmic Reticulum Stress/reactive Oxygen Species/nuclear Factor Kappa B Axis

Protein Tyrosine Phosphatase 1b And Insulin Resistance: Role Of Endoplasmic Reticulum Stress/reactive Oxygen Species/nuclear Factor Kappa B Axis

Protein Tyrosine Phosphatase 1B and Insulin Resistance: Role of Endoplasmic Reticulum Stress/Reactive Oxygen Species/Nuclear Factor Kappa B Axis Evgeniy Panzhinskiy , Jun Ren , Sreejayan Nair Affiliation: School of Pharmacy & Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, Wyoming, United States of America Affiliation: School of Pharmacy & Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, Wyoming, United States of America Affiliation: School of Pharmacy & Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, Wyoming, United States of America Obesity-induced endoplasmic reticulum (ER) stress has been proposed as an important pathway in the development of insulin resistance. Protein-tyrosine phosphatase 1B (PTP1B) is a negative regulator of insulin signaling and is tethered to the ER-membrane. The aim of the study was to determine the mechanisms involved in the crosstalk between ER-stress and PTP1B. PTP1B whole body knockout and C57BL/6J mice were subjected to a high-fat or normal chow-diet for 20 weeks. High-fat diet feeding induced body weight gain, increased adiposity, systemic glucose intolerance, and hepatic steatosis were attenuated by PTP1B deletion. High-fat diet- fed PTP1B knockout mice also exhibited improved glucose uptake measured using [3H]-2-deoxy-glucose incorporation assay and Akt phosphorylation in the skeletal muscle tissue, compared to their wild-type control mice which received similar diet. High-fat diet-induced upregulation of glucose-regulated protein-78, phosphorylation of eukaryotic initiation factor 2 and c-Jun NH2-terminal kinase-2 were sig Continue reading >>

Sfrbm: News

Sfrbm: News

Insulin Found to Control Cardiac Function Through Reactive Oxygen Species More than 30 million Americans have diabetes, according to the American Diabetes Association. A recent breakthrough by a Harvard School of Medicine research team has now shown that insulin may also impact the body in a unique way. The study ( ), led by Dr. Thomas Michel, of Harvard Medical School and Brigham and Womens Hospital, was recently published in Free Radical Biology and Medicine , a journal of the Society for Redox Biology and Medicine (SfRBM). The study was also recently highlighted in the Brigham and Womens Hospitals Clinical & Research News ( ). This new discovery unveiled an entirely unexpected mechanism whereby insulin-dependent generation of hydrogen peroxide (H2O2) in cardiac myocytes controls heart contractility and critical cell signaling pathways. These research findings have direct implications for our understanding of diabetic cardiomyopathy, which is a major cause of morbidity and mortality for patients with diabetes. Dr. Michel, a Professor of Medicine and Biochemistry and an SfRBM member said, These experiments reveal a new and unexpected role of H2O2 as a critical mediator of the physiological effects of insulin in the heart. We usually think of H2O2 as a harmful molecule that can cause pathological oxidative stress in diabetes and other diseases. Our recent discoveries help to establish that H2O2 actually plays a central role in modulating insulin action in the normal heart. We now need to more fully understand the factors that govern the transition from the physiological roles of H2O2 in normal cells to the pathological roles of H2O2 and related molecules in disease states. Michels team first observed that insulin treatment attenuated the usual response seen when adrena Continue reading >>

The Connection Between Oxygen And Diabetes

The Connection Between Oxygen And Diabetes

A lack of O2 in fat cells triggers inflammation and insulin resistance in obesity Researchers at the University of California, San Diego School of Medicine have, for the first time, described the sequence of early cellular responses to a high-fat diet, one that can result in obesity-induced insulin resistance and diabetes. The findings, published in the June 5 issue of Cell, also suggest potential molecular targets for preventing or reversing the process. “We’ve described the etiology of obesity-related diabetes. We’ve pinpointed the steps, the way the whole thing happens,” said Jerrold M. Olefsky, MD, associate dean for Scientific Affairs and Distinguished Professor of Medicine at UC San Diego. “The research is in mice, but the evidence suggests that the processes are comparable in humans and these findings are important to not just understanding how diabetes begins, but how better to treat and prevent it.” More than 25 million Americans have diabetes – 8.3 percent of the population – with another 79 million Americans estimated to be pre-diabetic, according to the American Diabetes Association. Diabetes is characterized by high blood sugar levels poorly regulated by either inadequate insulin production or because cells to not respond properly to the regulating hormone. Diabetes is the seventh leading cause of death in the United States and a major risk factor for other life-threatening conditions, including heart disease and stroke. Past research by Olefsky and others has shown that obesity is characterized by low-grade inflammation in adipose or fat tissues and that this inflammatory state can become chronic and result in systemic insulin resistance and diabetes. In today’s Cell paper, the scientists describe the earliest stages of the process, which Continue reading >>

An Adverse Effect Of Insulin On The Oxygen-release Capacity Of Red Blood Cells In Nonacidotic Diabetics

An Adverse Effect Of Insulin On The Oxygen-release Capacity Of Red Blood Cells In Nonacidotic Diabetics

Get rights and content Oxyhemoglobin dissociation curves (ODC) were performed on blood from newly diagnosed, nonketotic diabetics prior to and following initial insulin treatment and from ambulatory juvenile diabetics before and after their usual morning insulin. In 10 newly discovered diabetics the average P50 at in vivo pH was normal prior to insulin (26.2 mm Hg), decreased to 24.5 mm Hg (p < 0.005) on the day following the initial insulin administration, and was within normal limits (26.9 mm Hg) when the diabetes was finally well controlled and red cell 2,3-diphosphoglycerate (2,3-DPG) had risen to elevated levels. Oxygen affinity of hemoglobin was closely correlated with the content of red cell 2,3-DPG (r = 0.61, p < 0.001) but was unrelated to the level of hemoglobin Alc. In 40 juvenile patients the average P50 was also normal prior to insulin administration but was significantly lower 34 hr after they had received their usual insulin dose (p < 0.001). The study indicates that insulin administration to diabetics with high blood glucose levels may lead to transient decreases in red cell 2,3-DPG and in oxygen-releasing capacity of the red blood cells. Continue reading >>

Research Finds Insulin Needs Oxygen To Work

Research Finds Insulin Needs Oxygen To Work

Research finds insulin needs oxygen to work Dan Martin, director of CASE Medicine, uses a specialized camera to measure blood flow under his tongue at the base camp on Mount Everest 17,300 feet up. Caudwell Xtreme Everest A group of British scientists who trekked up Mount Everest has shed new light on how low levels of oxygen in the blood contribute to insulin resistance and adult-onset diabetes. The researchers used the highest mountain in the world as a laboratory to observe changes in 24 healthy subjects as the levels of oxygen in their blood dropped, instead of studying people at sea level already suffering insulin resistance and Type 2 diabetes. Insulin resistance, a precursor to full-blown diabetes, develops when cells in the body reject its own insulin, the hormone that regulates blood sugar. The pancreas then produces more insulin, and the resulting overload can cause damage to the heart, blood vessels, eyes, brain and other organs. The researchers found that healthy people who spent eight weeks on Mount Everest started to develop the same signs of insulin resistance found in people who are overweight or obese. "Fat tissue in obese people is believed to exist in a chronic state of mild hypoxia (low oxygen levels) because the small blood vessels are unable to supply sufficient oxygen to fat tissue," according to Mike Grocott, a professor at the University of Southampton, who co-founded of the Centre for Altitude, Space and Extreme environment medicine (CASE Medicine), which coordinated the research on Mount Everest. The Everest researchers, from the University of Southampton and University College London, reported their findings in the journal PLoS One. At sea level, blood oxygen saturation typically hovers around 98 percent. By the time the study subjects reach Continue reading >>

Is Oxygen Key To Insulin Resistance?

Is Oxygen Key To Insulin Resistance?

Oxygen is key to life but could it also be a key factor in insulin resistance and type 2 diabetes? We take a look at the evidence behind this idea and also which methods could use oxygen towards our advantage in tackling insulin resistance. A 2014 study found a link between the lack of oxygen on Everest and insulin resistance. Some research studies appear to show quite conclusively that restricting oxygen intake does indeed result in increased insulin resistance. A study carried out by researchers from the University of Southampton and University College London, published in 2014, investigated the effects of low oxygen levels on insulin resistance by taking adults up Mount Everest. The researchers found that as the participants reached higher altitudes, and were thus exposed to low levels of oxygen to breathe, they developed insulin resistance. Oxygen chamber improves insulin sensitivity By contrast, the opposite effect has also been observed. Researchers from the University of Adelaide tested the effects by exposing people with type 2 diabetes to a total of six periods of 90 minutes of hyperbaric oxygen therapy over a five-week period. Hyperbaric oxygen therapy involves spending time in a pressurised diving chamber containing 100% oxygen. The technique resulted in a dramatic 40% improvement in insulin sensitivity, an effect that would usually require a 13% loss of body weight. It seems apparent from this that the more oxygen we get, the better insulin sensitivity we have. Could oxygen also explain why people get insulin resistance in normal life at normal non-mountainous altitudes? It is notable that sleep apnea, a problem that results in disrupted breathing during sleep, is very closely related with type 2 diabetes. Sleep apnea shares obesity as a common major risk f Continue reading >>

Implantable Islet Cells Come With Their Own Oxygen Supply

Implantable Islet Cells Come With Their Own Oxygen Supply

Implantable islet cells come with their own oxygen supply Device could help insulin-producing cells live longer after transplant and improve treatment of type 1 diabetes. Media can only be downloaded from the desktop version of this website. Since the 1960s, researchers have been interested in the possibility of treating type 1 diabetes by transplanting islet cells the pancreatic cells that are responsible for producing insulin when blood glucose concentration increases. Implementing this approach has proven challenging, however. One obstacle is that once the islets are transplanted, they will die if they dont receive an adequate supply of oxygen. Now, researchers at MIT, working with a company called Beta-O2 Technologies, have developed and tested an implantable device that furnishes islet cells with their own supply of oxygen, via a chamber that can be replenished every 24 hours. Getting oxygen to these cells is a difficult problem, says Clark Colton, an MIT professor of chemical engineering and the senior author of the study. The benefits of this approach are: you keep the islets alive to perform their function, you dont need as much tissue, and you reduce the ability of the implants to provoke an immune response. Tests of these implants in rats showed that nearly 90 percent of the islets remained viable for several months, and most of the rats maintained normal blood glucose levels throughout that time. Yoav Evron of Beta-O2 Technologies is the lead author of the study, which appears in the April 25 issue of Scientific Reports. Type 1 diabetes occurs when a patients own immune system destroys pancreas islet cells, so the patient can no longer produce insulin, which is necessary for the body to absorb sugar from the bloodstream. Early attempts to treat patients by t Continue reading >>

The Contribution Of Singlet Oxygen To Insulin Resistance

The Contribution Of Singlet Oxygen To Insulin Resistance

The Contribution of Singlet Oxygen to Insulin Resistance Department of Food Science and Technology, Jomo Kenyatta University of Agriculture and Technology, P.O. Box 62000, Nairobi 00200, Kenya Department of Food Science and Technology, Jomo Kenyatta University of Agriculture and Technology, P.O. Box 62000, Nairobi 00200, Kenya Received 2017 Apr 24; Accepted 2017 Aug 7. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC. Insulin resistance contributes to the development of diabetes and cardiovascular dysfunctions. Recent studies showed that elevated singlet oxygen-mediated lipid peroxidation precedes and predicts diet-induced insulin resistance (IR), and neutrophils were suggested to be responsible for such singlet oxygen production. This review highlights literature suggesting that insulin-responsive cells such as endothelial cells, hepatocytes, adipocytes, and myocytes also produce singlet oxygen, which contributes to insulin resistance, for example, by generating bioactive aldehydes, inducing endoplasmic reticulum (ER) stress, and modifying mitochondrial DNA. In these cells, nutrient overload leads to the activation of Toll-like receptor 4 and other receptors, leading to the production of both peroxynitrite and hydrogen peroxide, which react to produce singlet oxygen. Cytochrome P450 2E1 and cytochrome c also contribute to singlet oxygen formation in the ER and mitochondria, respectively. Endothelial cell-derived singlet oxygen is suggested to mediate the formation of oxidized low-density lipoprotein which perpetuates IR, partly through neutrophil recrui Continue reading >>

Repetitive Hyperbaric Oxygen Treatment Increases Insulin Sensitivity In Diabetes Patients With Acute Intracerebral Hemorrhage

Repetitive Hyperbaric Oxygen Treatment Increases Insulin Sensitivity In Diabetes Patients With Acute Intracerebral Hemorrhage

Editor who approved publication: Professor Wai Kwong Tang Qian Xu, Yi-ting Wei, Shuang-bo Fan, Liang Wang, Xiao-ping Zhou Department of Brain Surgery, Ningbo Zhenhai Longsai Hospital, Zhejiang, Peoples Republic of China Aim: 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. Methods: 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 (80mUm-2min-1) at baseline and 10 and 30days after HBOT sessions. Serum insulin, fasting glucose, and hemoglobin A1C were measured in fasting serum at baseline and after HBOT sessions. In addition, early (~10days after onset) and late (1month after onset) outcomes (National Institutes of Health Stroke Scale, NIHSS scores) and efficacy (changes of NIHSS scores) of HBOT were evaluated. Results: In response to HBOT, the glucose infusion rate was increased by 37.8%5.76% at 1month 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 10days and 1month after onset (P<0.05). Conclusion: Peripheral insulin sensitivity was increased following HBOT in type 2 diabetes pa Continue reading >>

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