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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Before permanent European colonization 2 centuries ago, Australian Aborigines were preagriculturalist hunter-gatherers who had adapted extraordinarily well to life in a variety of habitats ranging from tropical forests, coastal and riverine environments, savannah woodlands, and grasslands to harsh, hot, and very arid deserts. Colonization had serious negative effects on Aboriginal society, well-being, and health, so much so that Aborigines are now the unhealthiest subgroup in Australian society. The change from active and lean hunter-gatherers to a more sedentary group of people whose diet is now predominantly Westernized has had, and continues to have, serious effects on their health, particularly in relation to cardiovascular disease and type 2 diabetes mellitus, which are highly prevalent among Aborigines. The contemporary diets of Australian Aborigines are energy rich and contain high amounts of fat, refined carbohydrates, and salt; they are also poor in fiber and certain nutrients, including folate, retinol, and vitamin E and other vitamins. Risks of development of cardiovascular disease and type 2 diabetes in this population probably develop during late childhood and adolescence. This indicates a need for greater emphasis on health promotion and disease prevention than at present and a need to plan these in culturally sensitive, secure, and appropriate ways. Most information about Aboriginal diets is anecdotal or semiquantitative. More effort needs to be invested in studies that more clearly and precisely define dietary patterns in Aboriginal people, especially children, and how these patterns influence their growth, nutritional status, and health, prospectively.
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PMID:Historical, cultural, political, and social influences on dietary patterns and nutrition in Australian Aboriginal children. 1106 78

Increased oxidative stress is believed to be an important factor in the development of diabetic complications. In this study, the effect of diabetes on the susceptibility of synaptosomes to oxidative stress, induced by the oxidizing system ascorbate/Fe2+, on the activity of antioxidant enzymes and on the levels of glutathione and vitamin E was investigated. Synaptosomes were isolated from brain of 29-weeks-old Goto-Kakizaki (GK) rats, a model of non-insulin dependent diabetes mellitus and from normal Wistar rats. Synaptosomes isolated from GK rats displayed a lower susceptibility to lipid peroxidation, as assessed by quantifying thiobarbituric acid reactive substances (TBARS), than normal rats (5.33 +/- 0.79 and 7.58 +/- 0.7 nmol TBARS/mg protein, respectively). In the absence of oxidants, no significant differences were found between the levels of peroxidation in synaptosomes of diabetic or control rats. Superoxide dismutase (SOD), glutathione peroxidase and glutathione reductase activities were unaltered in the brain of diabetic rats. There were no statistically significant differences in fatty acid composition of total lipids and reduced glutathione levels in synaptosomes of diabetic and control rats. The decreased susceptibility to membrane lipid peroxidation of diabetic rats synaptosomes correlated with a 1.3-fold increase in synaptosomal vitamin E levels. Vitamin E levels in plasma were also higher in diabetic rats (21.32 micromol/l) as compared to normal rats (15.13 micromol/l). We conclude that the increased resistance to lipid peroxidation in GK rat brain synaptosomes may be due to the increased vitamin E content, suggesting that diabetic animals might develop enhanced defense systems against brain oxidative stress.
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PMID:Synaptosomes isolated from Goto-Kakizaki diabetic rat brain exhibit increased resistance to oxidative stress: role of vitamin E. 1112 43

Previous studies hypothesised that vitamin E could protect against coronary heart disease and vascular complications in diabetes, but no studies have been performed regarding its eventual effects on fibrinolysis. Nevertheless, in Type 2 diabetes mellitus (T2DM) a profound reduction in the fibrinolytic activity has been demonstrated to be involved in vascular complications, probably due to plasminogen activator inhibitor type 1 (PAI-1) overproduction. On this basis we aimed to verify whether an antioxidant treatment with vitamin E is able to lower PAI-1 plasma levels in T2DM. Thirteen T2DM patients (9 males and 4 females; mean age+/-SD, 64.4+/-3.3 yr) were selected through strict admission criteria. These patients were treated with vitamin E (500 IU/die) for 10 weeks. Glyco-lipometabolic, oxidative and haemocoagulative parameters were evaluated at baseline and after 5, 10, 30 and 60 weeks. Vitamin E levels at different times were [median (interquartile range)] 6.1 (5.3-7.7), 8.5 (7.3-9.9), 9.7 (8.9-12.9), 5.6 (4.4-6.8), 5.7 (4.5-7.1) microg/ml, respectively. Significant differences were found for PAI-1 antigen (p=0.006), PAI-1 activity (p=0.028), apolipoprotein B (p=0.015) and antioxidant defence, evaluated as ferric reducing ability of plasma (FRAP) values (p=0.005). Particularly, decrements were detected for PAI-1 antigen between baseline and the 10th week (p<0.05), followed by an increase back to basal at the 30th week. Similar behaviour was found for PAI-1 activity. Regarding the antioxidant defence, FRAP values increased until the 30th week (p<0.05) with a decrease at the 60th week. These results demonstrate that vitamin E is able to lower PAI-1 levels in diabetic patients but this effect does not seem related to improvements of glycometabolic data or to the increase in FRAP values, suggesting that PAI-1 overproduction can be decreased by other effects of vitamin E on endothelial cells.
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PMID:Vitamin E intake reduces plasminogen activator inhibitor type 1 in T2DM patients. 1138 76

Type 2 diabetes, or non-insulin dependent diabetes mellitus (NIDDM), is increasingly common throughout the world. The World Health Organization has predicted that between 1997 and 2025, the number of diabetics will double from 143 million to about 300 million. The incidence of NIDDM is highest in economically developed nations, particularly the U.S., where approximately 6.5% of the population (17 million people) have either diagnosed or undiagnosed diabetes. The two most important factors contributing to the development of NIDDM are obesity and physical inactivity. The leading cause of mortality and morbidity in people with NIDDM is cardiovascular disease caused by macro- and microvascular degeneration. Current therapies for NIDDM focus primarily on weight reduction. Indeed, several investigations indicate that 65% to 75% of cases of diabetes in Caucasians could be avoided if individuals in this subgroup did not exceed their ideal weight. The success of this approach has been, at best, modest. An alternate approach to the control of Type 2 diabetes is to arrest the progress of the pathology until a cure has been found. To this end, some investigators suggest that dietary antioxidants may be of value. Several studies in humans and laboratory animals with NIDDM indicate that vitamin E and lipoic acid supplements lessen the impact of oxidative damage caused by dysregulation of glucose metabolism. In this brief review, we discuss the incidence, etiology, and current therapies for NIDDM and further explore the usefulness of dietary antioxidants in treating this disorder.
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PMID:Use of antioxidant nutrients in the prevention and treatment of type 2 diabetes. 1160 45

Free radical-mediated oxidative stress has been implicated in adverse tissue changes in a number of diseases. In view of the role of oxidative processes in non-insulin dependent diabetes mellitus (NIDDM), in this study, we investigated the oxidant and antioxidant status of plasma in patients with NIDDM and the effect of vitamin E (800 lU/day) supplementation on oxidative stress, antioxidant defense system, fructosamine levels and insulin action. Thirty controls and 40 NIDDM patients were studied. In controls and patients, plasma lipids, vitamin E, lipid peroxide, total thiols (t-SH), superoxide peroxidase (SOD) and glutathione peroxidase (GPx) were measured in the basal state and after vitamin E (800 IU/d) supplementation for a month. All lipids and lipid fractions in plasma were significantly decreased, whereas the HDL-C level was changed in diabetic patients supplemented with vitamin E when compared with baseline values. Vitamin E administration also significantly reduced fasting glucose and fructosamine levels, whereas increased significantly reduced fasting glucose and fructosamine levels, whereas increased significantly plasma C-peptide and insulin levels (p < 0.01, p < 0.001, respectively). Following vitamin E supplementation, TBARs levels were found to be significantly lower (p < 0.001) than the baseline value NIDDM patients are. On the other hand, activities of GPx and SOD were significantly higher (p < 0.001) than baseline values. A similar trend was observed for total thiols contents, but in this case, the increase was not significant. In conclusion, this study demonstrates that vitamin E improved beta-cell function and increased plasma insulin and C-peptide levels, possibly by inducing the antioxidant capacity of the organism and/or reducing the peripheral resistance in NIDDM. Long-term studies are needed to demonstrate the beneficial effects of vitamin E on treatment/prevention of NIDDM.
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PMID:Oxidant and antioxidant systems in niddm patients: influence of vitamin E supplementation. 1167 85

Nonalcoholic fatty liver disease is now recognized as the most common liver disease in the United States, with a prevalence of approximately 5% in the general population and up to 25% to 75% in patients with obesity and type II diabetes mellitus. Nonalcoholic fatty liver disease is a clinicopathologic syndrome with a wide spectrum of histologic abnormalities and clinical outcomes. Hepatic steatosis has a benign clinical course. In contrast, nonalcoholic steatohepatitis (NASH) may progress to cirrhosis and liver-related death in 25% and 10% of patients, respectively. Cases occur most commonly in obese, middle-aged women with diabetes. However, NASH may also occur in children and normal-weight men with normal glucose and lipid metabolism. The pathophysiology involves two steps. The first is insulin resistance, which causes steatosis. The second is oxidative stress, which produces lipid peroxidation and activates inflammatory cytokines resulting in NASH. Liver biopsy provides prognostic information and identifies NASH patients who may benefit from therapy. Treatment consists of managing the comorbidities: obesity, diabetes, and hyperlipidemia. Although antioxidant therapy with vitamin E is often used, ursodeoxycholic acid is the only drug that has shown benefit and is the most promising of the drugs currently being investigated. Future therapies will depend on a greater understanding of the pathophysiology and should focus on diminishing fibrosis.
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PMID:Update on nonalcoholic fatty liver disease. 1187 8

Morbid obesity (BMI > or = 40 kg/m2) is accompanied by lipid disturbances which may be involved in the increased incidence of arterial hypertension and non-insulin dependent diabetes mellitus. The aim of the study was to assess plasma concentrations of total cholesterol (TC), HDL-cholesterol, LDL-cholesterol, triglycerides (TG) and two parameters of oxidation stress--vitamin E and oxysterols, in morbidly obese patients with coexisting arterial hypertension and non-insulin dependent diabetes mellitus. Studies were performed in 37 morbidly obese patients divided into three groups: group I--without coexisting diseases, group II--with arterial hypertension, and group III--with arterial hypertension and non-insulin dependent diabetes mellitus. In all groups there was an increase in TG concentration, a decrease in HDL-cholesterol level, and normal values of TC and LDL-cholesterol. The concentrations of 7-hydroxycholesterols (7-OH) in group II (602.65 +/- 264.46 ng/ml) and group III (570.94 +/- 210.59 ng/ml) were significantly higher compared to that in group I (336.09 +/- 220.74 ng/ml). There were no differences between groups in concentrations of 7-ketocholesterols (7-K), TC, HDL-cholesterol, LDL-cholesterol, TG, vitamin E and vitamin E/(TC + TG) ratio. In all groups TC concentration correlated positively with TG concentration, and negatively with vitamin E/(TC + TG) ratio. Moreover, the positive correlation between TG and HDL-cholesterol concentrations, and negative correlation between plasma vitamin E and 7-K concentrations were demonstrated. In conclusion, although the study demonstrates similar disturbances in lipid profile and oxidation stress parameters in all groups, with significant differences in 7-OH only, the role of cholesterol oxidation products in pathogenesis of arterial hypertension and non-insulin dependent diabetes mellitus in morbidly obese patients cannot be excluded.
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PMID:[Assessment of plasma lipid profile oxysterols and vitamin E concentration in morbidity obese patients with coexisting arterial hypertension and non-insulin dependent diabetes mellitus]. 1210 69

Endothelial dysfunction has been proposed as an early manifestation of atherosclerosis. The risk for atherosclerosis is increased in patients with diabetes mellitus, but the mechanism of the increased risk in these patients remains to be elucidated. Emerging evidence suggests that postprandial hyperglycaemia and hyperlipidemia are important risk factors in the development of atherosclerosis in patients with diabetes. Using a high-resolution ultrasound technique, we evaluated the acute effects of oral glucose loading on endothelium-dependent flow-mediated dilation (EFMD) and endothelium-independent flow-mediated dilation (EIFMD) of the brachial artery in 11 men (mean age: 59 +/- 5 years) with type 2 diabetes without chronic complications of diabetes. During these examinations, changes in the level of superoxide anion formation in the neutrophils were also measured. In addition, to investigate the relationship between acute hypertriglyceridemia and EFMD, we assessed the effects of high- and low-fat meals on EFMD of the brachial artery in 12 healthy volunteers. EFMD was diminished after glucose loading (13.2% +/- 6.4%, 7.3% +/- 3.3%*, 12.8% +/- 5.6%, in fasting and at 1 and 2 hours, respectively; *P<0.001 vs fasting). Superoxide anion formation by neutrophils (expressed as 10(-7) nmol/10(6) cells/30 min) was increased after glucose loading (4.7 +/- 2.8 and 6.2 +/- 2.2, in fasting and at one hour, respectively; P<0.05). EIFMD and triglyceride concentrations were not significantly affected by glucose loading. EFMD was also decreased by high-fat feeding (13.1% +/- 4.3%, 7.7% +/- 3.7%*, 7.3% +/- 2.2%*, basal, 2 hours, and 4 hours, respectively; *P<0.01 vs basal). These decreases were reversed by vitamin E treatment. These results show that acute hyperglycaemia induced by 75 gm oral glucose intake and acute hypertriglyceridemia induced by high-fat feeding are implicated in endothelial dysfunction. In addition, these results suggest that chronic and repeated hyperglycaemia and hypertriglyceridemia may play important roles in the development and progression of vascular complications in diabetes, probably through increased oxidative stress.
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PMID:Endothelial dysfunction: its relationship with acute hyperglycaemia and hyperlipidemia. 1216 9

Nonalcoholic fatty liver disease (NAFLD) includes a wide spectrum of liver injury ranging from simple steatosis to steatohepatitis, fibrosis, and cirrhosis. Whereas simple steatosis has a benign clinical course, steatohepatitis is a recognized cause of progressive liver fibrosis and can develop into cirrhosis. NAFLD and nonalcoholic steatohepatitis (NASH) are the two most common chronic liver diseases in United States general population with a prevalence of 20% and 3%, respectively. Hepatic steatosis is frequently associated with obesity, type 2 diabetes, and hyperlipidemia with insulin resistance as a key pathogenic factor. A two-hit theory best describes the progression from simple steatosis to NASH, fibrosis, or cirrhosis. These two hits consist of the accumulation of excessive hepatic fat primarily owing to insulin resistance, and oxidative stress owing to reactive oxygen species (ROS). Mitochondria are the major cellular source of ROS in cases of NASH. Currently, treatment is focused on modifying risk factors such as obesity, diabetes mellitus, and hyperlipidemia. Antioxidants such as vitamin E, N-acetylcysteine, betaine, and others may be beneficial in the treatment of NASH.
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PMID:Nonalcoholic fatty liver disease: pathogenesis and the role of antioxidants. 1229 56

In both type 1 and type 2 diabetes, the late diabetic complications in nerve, vascular endothelium, and kidney arise from chronic elevations of glucose and possibly other metabolites including free fatty acids (FFA). Recent evidence suggests that common stress-activated signaling pathways such as nuclear factor-kappaB, p38 MAPK, and NH2-terminal Jun kinases/stress-activated protein kinases underlie the development of these late diabetic complications. In addition, in type 2 diabetes, there is evidence that the activation of these same stress pathways by glucose and possibly FFA leads to both insulin resistance and impaired insulin secretion. Thus, we propose a unifying hypothesis whereby hyperglycemia and FFA-induced activation of the nuclear factor-kappaB, p38 MAPK, and NH2-terminal Jun kinases/stress-activated protein kinases stress pathways, along with the activation of the advanced glycosylation end-products/receptor for advanced glycosylation end-products, protein kinase C, and sorbitol stress pathways, plays a key role in causing late complications in type 1 and type 2 diabetes, along with insulin resistance and impaired insulin secretion in type 2 diabetes. Studies with antioxidants such as vitamin E, alpha-lipoic acid, and N-acetylcysteine suggest that new strategies may become available to treat these conditions.
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PMID:Oxidative stress and stress-activated signaling pathways: a unifying hypothesis of type 2 diabetes. 1237 42


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