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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The annual sale of x-ray contrast media (CM) now represents 60 million doses, and contrast nephropathy (CN) has been the third-leading cause of hospital-acquired acute renal failure. In this review article, physicochemical, pharmacokinetic, and pharmacodynamic properties of CM are surveyed. The definition of CN is presented, as well as the mechanisms involved in the pathogenesis. Low osmolar monomeric CM (LOCM) are less nephrotoxic than the older ionic high osmolar CM (HOCM), but in risk patients the incidence of CN is still high after intravascular administration of LOCM. Non-ionic dimeric CM are iso-osmolar to plasma (IOCM), and they have reduced the nephrotoxicity even more than LOCM. The most important risk factors for CN are diabetes mellitus and impaired renal function. Selection of patients, hydration, and type of CM are essential for prevention and prophylaxis of CN. We do not recommend routine prophylaxis with N-acetylcysteine (NAC) during CM investigations, but its use in high-risk patients should be considered.
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PMID:Nephrotoxic effects of X-ray contrast media. 1536 4

Diabetic retinopathy is a leading cause of blindness and one of the hallmarks of early diabetic retinopathy is death of pericytes. I studied the effect of glycated albumin (GA) on the retinal pericyte death and assessed the protective effects of some well-known antioxidant materials. GA produced a progressive cytotoxic effect in a near time and dose dependent manner. Among the antioxidant pretreatments, L-ascorbic acid, Trolox, produced a reduction of GA-induced cytototoxicity. N-Acetyl-L-cysteine showed partial effect but taurine had no effect on the GA-toxicity. In conclusion, I demonstrated the effect of GA on the retinal pericyte death and some antioxidants effectively prevented the GA-induced cell death in pericytes.
Diabetes Res Clin Pract 2004 Dec
PMID:Pericytes and the prevention of diabetic retinopathy. 1556 80

Insulin action is impaired in diabetic patients, which leads to increased hepatic glucose production. Plants and herbs have been used for medicinal purposes, including the treatment of diabetes, for centuries. Since dietary management is a starting point for the treatment of diabetes, it is important to recognize the effect of plant-based compounds on tissues that regulate glucose metabolism, such as the liver. In a recent study, several herbs and spices were found to increase glucose uptake into adipocytes, an insulin-like effect. Our data reveal that Syzygium aromaticum (L.) Merrill and Perry (Myrtaceae) (commonly referred to as clove) extract acts like insulin in hepatocytes and hepatoma cells by reducing phosphoenolpyruvate carboxykinase (PEPCK) and glucose 6-phosphatase (G6Pase) gene expression. Much like insulin, clove-mediated repression is reversed by PI3K inhibitors and N-acetylcysteine (NAC). A more global analysis of gene expression by DNA microarray analysis reveals that clove and insulin regulate the expression of many of the same genes in a similar manner. These results demonstrate that consumption of certain plant-based diets may have beneficial effects for the treatment of diabetes and indicate a potential role for compounds derived from clove as insulin-mimetic agents.
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PMID:An extract of Syzygium aromaticum represses genes encoding hepatic gluconeogenic enzymes. 1558 82

Individuals with Down syndrome have signs of possible brain damage prior to birth. In addition to slowed and reduced mental development, they are much more likely to have cognitive deterioration and develop dementia at an earlier age than individuals without Down syndrome. Some of the cognitive impairments are likely due to post-natal hydrogen peroxide-mediated oxidative stress caused by overexpression of the superoxide dismutase (SOD-1) gene, which is located on the triplicated 21st chromosome and known to be 50% overexpressed. However, some of this disability may also be due to early accumulation of advanced protein glycation end-products, which may play an adverse role in prenatal and postnatal brain development. This paper suggests that essential nutrients such as folate, vitamin B6, vitamin C, vitamin E, selenium, and zinc, as well as alpha-lipoic acid and carnosine may possibly be partially preventive. Acetyl-L-carnitine, aminoguanidine, cysteine, and N-acetylcysteine are also discussed, but have possible safety concerns for this population. This paper hypothesizes that nutritional factors begun prenatally, in early infancy, or later may prevent or delay the onset of dementia in the Down syndrome population. Further examination of these data may provide insights into nutritional, metabolic and pharmacological treatments for dementias of many kinds. As the Down syndrome population may be the largest identifiable group at increased risk for developing dementia, clinical research to verify the possible validity of the prophylactic use of anti-glycation nutrients should be performed. Such research might also help those with glycation complications associated with diabetes or Alzheimer's.
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PMID:Can cognitive deterioration associated with Down syndrome be reduced? 1561 60

Contrast-induced nephropathy (CIN) is a leading cause of in-hospital acute renal failure in critically ill patients who undergo radiographic procedures. Critical care patients are at particular risk, often because of baseline renal dysfunction, older age, and the presence of diabetes. In addition, there are superimposed risks, including volume depletion, sepsis, and use of nephrotoxic drugs. The rates of CIN (defined as an increase in serum creatinine by >25% or 0.5 mg/dL) can be predicted by using multivariate tools. Prevention measures include adequate hydration, use of N-acetylcysteine and iso-osmolar contrast, and for patients who are at the highest risk, prophylactic hemofiltration.
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PMID:Contrast-induced nephropathy. 1578 Nov 62

The intravascular administration of iodinated radiocontrast media can lead to acute renal dysfunction. Even small changes in renal function have been associated with increased morbidity and mortality, making the prevention of radiocontrast nephropathy of paramount importance. This review summarizes the principal risk factors for radiocontrast nephropathy and evidence-based preventive strategies that should be used to limit its occurrence. Risk factors for radiocontrast nephropathy include preexistent kidney disease, diabetes mellitus, dose of radiocontrast used, advanced congestive heart failure, and intravascular volume depletion. Proven preventive measures include volume expansion with intravenous saline or sodium bicarbonate and the use of low-osmolar or iso-osmolar radiocontrast media. Studies evaluating N-acetylcysteine have been conflicting, with meta-analyses suggesting a small beneficial effect. Studies of other pharmacologic agents have not demonstrated clinical benefit.
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PMID:Radiocontrast-induced acute renal failure. 1585 19

Contrast media-induced nephropathy is the third most common cause of hospital acquired acute renal failure. With the increasing use of contrast media in diagnostic and interventional procedures it has become one of the major challenges encountered during routine cardiology practice. Despite clinical importance it is an under-recognized event with major morbidity and mortality. Risk of developing contrast media-induced nephropathy depends mainly on patients preexisting characteristics and physicochemical properties of the contrast agent. Primary attempts for the prevention of contrast media-induced nephropathy should include systematic review of patient's characteristics and risk stratification. Patients at the greatest risk for contrast media-induced nephropathy can be defined as those having preexisting impaired renal function, diabetes mellitus, and congestive heart failure. Other risk factors include; age above seventy years, female gender, dehydration and use of high volume contrast media. The more expeditious use of iso-osmolar non-ionic contrast media reduced the incidence of contrast media related renal dysfunction. Currently, the only widely proven method of reducing the risk of contrast-induced nephropathy is adequate pre and postprocedural hydration. In addition, prophylactic use of free radical scavenger N-acetylcysteine has been shown to prevent contrast media-induced nephropathy in some moderate-scale clinical trials and a meta-analysis. Despite the attempts to reduce the risk of contrast nephropathy, this clinical event affects over 25% of high risk patients and mortality remains to be high.
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PMID:[Contrast media-induced nephropathy: clinical burden and current attempts for prevention]. 1593 88

We examined if myocardial depression at the acute phase of diabetes (3 weeks after injection of streptozotocin, 60 mg/kg i.v.) is due to activation of inducible nitric oxide synthase and production of peroxynitrite, and if treatment with N-acetylcysteine (1.2 g/day/kg for 3 weeks, antioxidant) improves cardiac function. Four groups of rats were used: control, N-acetylcysteine-treated control, diabetic and N-acetylcysteine-treated diabetic. Pentobarbital-anaesthetized diabetic rats, relative to the controls, had reduced left ventricular contractility to dobutamine (1-57 microg/min/kg). The diabetic rats also had increased myocardial levels of thiobarbituric acid reactive substances, immunostaining of inducible nitric oxide synthase and nitrotyrosine, and similar baseline 15-F2t-isoprostane. N-acetylcysteine did not affect responses in the control rats; but increased cardiac contractility to dobutamine, reduced myocardial immunostaining of inducible nitric oxide synthase and nitrotyrosine and level of 15-F2t-isoprostane, and increased cardiac contractility to dobutamine in the diabetic rats. Antioxidant supplementation in diabetes reduces oxidative stress and improves cardiac function.
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PMID:The effect of N-acetylcysteine on cardiac contractility to dobutamine in rats with streptozotocin-induced diabetes. 1611 76

Podocytes or glomerular epithelial cells (GECs) are important targets of the diabetic microenvironment. Podocyte foot process effacement and widening, loss of GECs and hypertrophy are pathological features of this disease. ANG II and oxidative stress are key mediators of renal hypertrophy in diabetes. The cellular mechanisms responsible for GEC hypertrophy in diabetes are incompletely characterized. We investigated the effect of high glucose on protein synthesis and GEC hypertrophy. Exposure of GECs to high glucose dose dependently stimulated [(3)H]leucine incorporation, but not [(3)H]thymidine incorporation. High glucose resulted in the activation of ERK1/2 and Akt/PKB. ERK1/2 pathway inhibitor or the dominant negative mutant of Akt/PKB inhibited high glucose-induced protein synthesis. High glucose elicited a rapid generation of reactive oxygen species (ROS). The stimulatory effect of high glucose on ROS production, ERK1/2, and Akt/PKB activation was prevented by the antioxidants catalase, diphenylene iodonium, and N-acetylcysteine. Exposure of the cells to hydrogen peroxide mimicked the effects of high glucose. In addition, ANG II resulted in the activation of ERK1/2 and Akt/PKB and GEC hypertrophy. Moreover, high glucose and ANG II exhibited additive effects on ERK1/2 and Akt/PKB activation as well as protein synthesis. These additive responses were abolished by treatment of the cells with the antioxidants. These data demonstrate that high glucose stimulates GEC hypertrophy through a ROS-dependent activation of ERK1/2 and Akt/PKB. Enhanced ROS generation accounts for the additive effects of high glucose and ANG II, suggesting that this signaling cascade contributes to GEC injury in diabetes.
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PMID:Redox dependence of glomerular epithelial cell hypertrophy in response to glucose. 1623 11

Increased oxidative stress and reduced nitric oxide (NO) bioactivity are key features of diabetes mellitus that eventually result in cardiovascular abnormalities. We assessed whether N-acetylcysteine (NAC), an antioxidant and glutathione precursor, could prevent the hyperglycaemia induced increase in oxidative stress, restore NO availability and prevent depression of arterial blood pressure and heart rate in vivo in experimental diabetes. Control (C) and streptozotocin-induced diabetic (D) rats were treated or not treated with NAC in drinking water for 8 weeks, initiated 1 week after induction of diabetes. At termination, plasma levels of free 15-F2t-isoprostane, a specific marker of oxygen free radical induced lipid peroxidation, was increased while the plasma total antioxidant concentration was decreased in untreated diabetic rats as compared to control rats (P<0.05). This was accompanied by a significant reduction of plasma levels of nitrate and nitrite, stable metabolites of NO, (P<0.05, D vs. C) and a reduced endothelial NO synthase protein expression in the heart and in aortic and mesenteric artery tissues. Systolic, diastolic and mean arterial blood pressures (SBP, DBP and MAP) and heart rate (HR) were reduced in diabetic rats (P<0.05 vs. C) and NAC normalised the changes that occurred in the diabetic rats. The protective effects may be attributable to restoration of NO bioavailability in the circulation.
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PMID:Antioxidant N-acetylcysteine restores systemic nitric oxide availability and corrects depressions in arterial blood pressure and heart rate in diabetic rats. 1639 Aug 27


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