Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Orthostatic hypertension--a rise in blood pressure upon assuming upright posture-is an underappreciated and understudied clinical phenomenon. There is currently no widely agreed-upon definition of clinical orthostatic hypertension, the current definitions being operational within the context of particular studies. The underlying pathophysiology is thought to involve activation of the sympathetic nervous system, but the actual etiology is poorly understood. Orthostatic hypertension is observed in association with a variety of other clinical conditions, including essential hypertension, dysautonomias, and type 2 diabetes mellitus. Orthostatic hypertension has been associated with increased occurrence of silent cerebrovascular ischemia and possibly with neuropathy in type 2 diabetes. So, appreciation of the true incidence of orthostatic hypertension, elucidation of the underlying pathophysiology, and an understanding of potentially effective treatment approaches and their associated risks and benefits might all have major clinical significance. Orthostatic hypertension is an aspect of hypertension that is in need of further focused investigation.
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PMID:Orthostatic hypertension: when pressor reflexes overcompensate. 1693 77

Autoimmune or type 1 diabetes mellitus (T1DM), accounts for 90-95% of all cases of diabetes, while type 2 diabetes mellitus (T2DM), characterized by impaired insulin sensitivity and production, accounts for the other 5-10%. Atherosclerotic process starts during childhood and recognize several mechanisms that are activated in response to NOXIUS STIMULI and participate in a complex state which is accepted to be a chronic inflammatory state. T1DM patients, especially those with a non-optimal metabolic control, have a higher risk of developing all macrovascular complications such as myocardial infarction, stroke and silent ischemia. Macrovascular disease is mainly associated with hyperglycemia, dyslipidemia, obesity, hypertension, hypercoagulable state, cigarette smoking, lack of exercise, endothelial dysfunction, hyperhomocysteinemia and vascular wall abnormalities. In this paper we review the importance of traditional and non-traditional risk factors for macrovascular complications in children with T1DM and discuss their role in the pathogenesis of the excess cardiovascular mortality in these patients.
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PMID:Macroangiopathy in adults and children with diabetes: risk factors (part 2). 1711 Dec 97

Hyperglycemia has been shown to worsen the outcome of brain ischemia in several animal models but few experimental studies have investigated impairments in cognition induced by ischemic brain lesions in hyperglycemic animals. The Goto-Kakizaki (GK) rat naturally develops type 2 diabetes characterized by mild hyperglycemia and insulin resistance. We hypothesized that GK rats would display more severe cerebral damage due to hyperglycemia-aggravated brain injury and, accordingly, more severe cognitive impairments. In this study, recovery of motor and cognitive functions of GK and healthy Wistar rats was examined following extradural compression (EC) of the sensorimotor cortex. For this purpose, tests of vestibulomotor function (beam-walking) and combined tests of motor function and learning (locomotor activity from day (D) 1 to D5, operant lever-pressing from D14 to D25) were used. EC consistently reduced cerebral blood flow in both strains. Anesthesia-challenge and EC resulted in pronounced hyperglycemia in GK but not in Wistar rats. Lower beam-walking scores, increased locomotor activity, impairments in long-term habituation and learning of operant lever-pressing were more pronounced and observed at later time-points in GK rats. Fluoro-Jade, a marker of irreversible neuronal degeneration, revealed consistent degeneration in the ipsilateral cortex, hippocampus and thalamus at 2, 7 and 14 days post-compression. The amount of degeneration in these structures was considerably higher in GK rats. Thus, GK rats exhibited marked hyperglycemia during EC, as well as longer-lasting behavioral deficits and increased neurodegeneration during recovery. The GK rat is thus an attractive model for neuropathologic and cognitive studies after ischemic brain injury in hyperglycemic rats.
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PMID:Diabetic Goto-Kakizaki rats display pronounced hyperglycemia and longer-lasting cognitive impairments following ischemia induced by cortical compression. 1717 9

The aim of this study is to identify the risk factors for development of chronic critical limb ischemia (CLI) in diabetic and nondiabetic patients with peripheral arterial disease (PAD). 127 patients (pts) with PAD (63 with type 2 diabetes and 64 nondiabetic) were randomly included in a cross sectional study. Out of them 17 were with CLI. Population was investigated for age, height, weight, sex, duration of PAD and diabetes, arterial hypertension, hyperlipidemia, smoking, obesity, systolic blood pressure, value of ankle-brachial index, previous claudicating distance and peripheral intervention, amputation, medical treatment with prostanoids, insulin and antiplatelet drugs and histories of cerebrovascular disease, coronary artery disease and other concomitant diseases. After adjudging linear correlation between mentioned variables and presence of CLI, logistic regression model was built. There were no significant differences in demographic data between both populations. Hyperlipidemia was more frequent in nondiabetic population. Multiple regression model show ankle-brachial index < 0,5, measured in previous 1-3 years (OR 3.39 CI 95% 0.28-40.78), microvascular complication retinopathy (OR 12.98 CI 95% 1.76-95.58), heart failure (OR 1.91 CI 95% 0.29-2.72) and previous prostanoids treatment (OR 15.92 CI 95% 0.53-476.58) as predictors of development of CLI in diabetic population with PAD. After heart failure exclusion of model of nondiabetic pts, previous surgery (OR 3.14 CI 95% 0.61-16.09) and smoking (OR 0.35 CI 95% 0.78-1.62) were presented as prognostic factors for CLI's onset. Our results indicate differences between predictors of CLI's onset in diabetic and nondiabetic population with PAD. Presence of retinopathy, previous measured ankle-brachial index and prostanoids treatment are predictors of development of CLI in diabetic population. Previous surgery is independent predictor for CLI'onset in nondiabetics. Treating concomitant heart failure for both populations and modifying risk factor smoking in nondiabetic population, have an important clinical usefulness in risk assessment approach of peripheral arterial disease patients.
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PMID:Risk factors for development of critical limb ischemia -- a survey of diabetic vs. nondiabetic population. 1721 Dec 94

Myocardial sarcolemmal ATP-dependent potassium (KATP) channels, which are normally closed by high ATP concentration, open during ischemia when ATP generation decreases favoring K(+) efflux. This reduces action potential duration (APD) decreasing the time of Ca(2+) influx and Ca(2+) overload. This behavior suggested that they might be involved in the protection against stunning and arrhythmias and in the mechanism of ischemic preconditioning. Sulfonylureas, used as hypoglycemic agents for the treatment of type 2 diabetes also block myocardial KATP channels prolonging APD during ischemia, which by allowing Ca(2+) entry for a longer period of time, is potentially harmful to the heart. Controversial findings have been reported regarding the protective effect of sulfonylureas. Due to their importance in the clinical setting, their action on the heart of large conscious animal models is relevant. The effect of glibenclamide, a representative sulfonylurea, has been studied in a conscious sheep model submitted to regional 12 min ischemia. Glibenclamide (0.4 mg/kg) completely blocked KATP channels, as assessed by monophasic APD, producing a deleterious effect on reperfusion-induced arrhythmias and myocardial recovery from stunning in normal animals. This adverse effect was more noticeable in alloxan-induced diabetic sheep, where a lower dose (0.1 mg/kg) inhibited KATP channel opening worsening mechanical recovery and arrhythmia incidence. However, glibenclamide did not abolish ischemic late preconditioning against stunning and arrhythmias in normal animals. Because diabetic sheep do not develop this cardioprotective phenomenon, probably due to KATP channel dysfunction, it was not possible to assess glibenclamide effect on preconditioning in this pathological condition. In conclusion, in large conscious animals, glibenclamide interferes with the beneficial action of KATP channel opening during acute ischemia-reperfusion events both in normal and diabetic animals. Therefore, despite some studies claiming no added cardiovascular risk due to glibenclamide treatment, this pharmacological agent should be further investigated to ensure its safe administration in patients with concurrent heart disease.
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PMID:Glibenclamide action on myocardial function and arrhythmia incidence in the healthy and diabetic heart. 1726 47

The aim of the investigation was to study the significance of the functional condition of endothelium for the evaluation of ischemic episodes in patients with type 2 diabetes mellitus (DM2). Ninety-three patients (52 men; 41 women; mean age 58.3+/-4.8 years) were examined. Group 1 consisted of 47 patients with coronary heart disease (CHD) and CD2; group 2 consisted of 46 CAD patients without carbohydrate exchange disorder. Both groups were comparable by gender, age, and the main risk factors. The patients were examined using Holter monitoring, physical load test, EchoCG, reactive hyperemia test (ultrasound evaluation of the endothelium-dependent brachial artery dilation). The number of painless ischemic episodes (PIE), the total duration of ischemia, the maximum degree of ST depression prevailed in group 1 patients. Correlation analysis demonstrated a significant negative correlation between endothelial dysfunction, one the one part, and the number and duration of PIE and the time between the ischemic ST depression and pain syndrome, on the other, in group 1 patients.
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PMID:[Clinicofunctional evaluation of ischemic episodes and vascular endothelium in patients with type 2 diabetes]. 1729 80

Acute cellular graft-vs.-host disease (GVHD) following liver transplantation has an incidence of 1 to 2% and a mortality rate of 85%. Our aim was to identify a patient population at high risk for developing GVHD using a large clinical database to study both recipient and donor factors. We compared our liver transplant patients who developed GVHD to those that did not for recipient and donor factors and combinations of factors. For 2003-2004 we had 205 first-time liver transplant patients surviving >30 days. From this group, 4 (1.9%) developed GVHD. Compared to the control group, there were no significant differences in recipient age, recipient gender, donor age, donor gender, total ischemia time, donor-recipient human leukocyte antigen (HLA) mismatch, or donor-recipient age difference. Percentages of liver disease etiologies among the patients who developed GVHD were as follows: 16% (1/6) autoimmune hepatitis (AIH) (P = 0.003), 5.6% (3/54) alcoholic liver disease (ALD) (P = 0.057), and 7.1% (3/42) hepatocellular carcinoma (HCC) (P = 0.026). The incidence of GVHD in patients with glucose intolerance (either Type I or Type II diabetes mellitus [DM]) was significant (P = 0.022). Focusing on patients only with high-risk factors for GVHD during the years 2003-2005, we had 19 such patients. Four of these high-risk patients developed GVHD. Three of these 4 patients had received a donor liver with steatosis of degree >or=mild compared to only 2 of the 15 high-risk patients who did not develop GVHD (P = 0.037). In conclusion, we have identified liver transplant patients with AIH or the combination of ALD, HCC, and glucose intolerance who receive a steatotic donor liver as being at high risk for developing GVHD.
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PMID:Recipient and donor factors influence the incidence of graft-vs.-host disease in liver transplant patients. 1739 49

In clinic, the patients with acute myocardial infarction (AMI) are at high risk to develop ischemia-induced ventricular arrhythmias leading to sudden cardiac death (SCD). Some studies suggest that individual susceptibility to ischemia-induced arrhythmia may be related to the genes encoding ion channels. One of them is the cardiac ATP-sensitive potassium channel (K(ATP)), which is an octamer composed of four pore-forming inwardly rectifying potassium-channel subunits (Kir6.2) and four regulatory sulfonylurea-receptor subunits (SUR2A). They play important roles in the physiology and pathophysiology of cardiovascular system by coupling the metabolic state of the cells to cellular electrical activity. So far, some mutations and polymorphisms of Kir6.2/KCNJ11 gene showed significant correlation with type 2 diabetes. But it was not sure whether it was associated with acute myocardial diseases. Hence a complete mutational analysis of Kir6.2/KCNJ11 gene was performed in a pedigree of sudden cardiac death. The complete coding region and the intron-exon boundaries of KCNJ11 were amplified from genomic DNA using polymerase chain reaction (PCR). Direct sequencing was done to identify any mutations and then further confirmed by restriction site polymorphism (RSP) approach. No mutation was detected in the samples analyzed, a common polymorphism K23E (A>G) was noticed in this pedigree and the proband showed a homozygote genotype (G/G). The result suggests that the Kir6.2/KCNJ11 gene is not related to sudden cardiac death in this family.
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PMID:Study of Kir6.2/KCNJ11 gene in a sudden cardiac death pedigree. 1743 20

The prognostic significance of myocardial ischemia assessed by dobutamine stress echocardiography in asymptomatic patients with diabetes mellitus who have no previous coronary artery disease remains unclear. We assessed the value of dobutamine stress echocardiography for risk stratification in 161 asymptomatic patients with type 2 diabetes (mean 62 +/- 12 years of age; 96 men) who had no previous myocardial infarction or revascularization. End point during follow-up was hard cardiac events (cardiac death and nonfatal myocardial infarction). Ischemia was detected in 45 patients (28%). During a median follow-up of 5 years, 40 patients (25%) died (18 cardiac deaths) and 7 patients had nonfatal myocardial infarction (25 hard cardiac events). An abnormal dobutamine stress echocardiogram was associated with a higher mortality compared with a normal dobutamine stress echocardiogram (p = 0.03). In an incremental multivariate analysis model, clinical predictors of hard cardiac events were age and hypercholesterolemia. Ischemia was incremental to the clinical parameters. In conclusion, myocardial ischemia is an independent predictor of cardiac events in asymptomatic diabetic patients with no previous coronary artery disease.
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PMID:Prognostic significance of myocardial ischemia during dobutamine stress echocardiography in asymptomatic patients with diabetes mellitus and no prior history of coronary events. 1747 39

Deteriorating islet beta-cell function is key in the progression of an impaired glucose tolerance state to overt type 2 diabetes (T2D), a transition that can be delayed by exercise. We have previously shown that trained rats are protected from heart ischemia-reperfusion injury in correlation with an increase in cardiac tissue fatty-acid oxidation. This trained metabolic phenotype, if induced in the islet, could also prevent beta-cell failure in the pathogenesis of T2D. To assess the effect of training on islet lipid metabolism and insulin secretion, female Sprague-Dawley rats were exercised on a treadmill for 90 min/d, 4 d/week, for 10 weeks. Islet fatty-acid oxidation, the expression of key lipid metabolism genes, and glucose-stimulated insulin secretion were determined in freshly isolated islets from trained and sedentary control rats after a 48 h rest period from the last exercise. Although this moderate training reduced plasma glycerol, free fatty acids, and triglyceride levels by about 40%, consistent with reduced lipolysis from adipose tissue, it did not alter islet fatty-acid oxidation, nor the islet expression of key transcription factors and enzymes of lipid metabolism. The training also had no effect on glucose-stimulated insulin secretion or its amplification by free fatty acids. In summary, chronic exercise training did not cause an intrinsic change in islet lipid metabolism. Training did, however, substantially reduce the exposure of islets to exogenous lipid, thereby providing a potential mechanism by which exercise can prevent islet beta-cell failure leading to T2D.
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PMID:Circulating lipids are lowered but pancreatic islet lipid metabolism and insulin secretion are unaltered in exercise-trained female rats. 1748 65


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