Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There are few studies on the effects of postprandial hyperglycaemia, and usually it is assumed that its effects are the same as those of post-glucose-load hyperglycaemia, following a standard 75 g oral glucose tolerance test. There is some evidence from a study with blood drawn following ingestion of a standardised "diabetes screening product" or a 75 g oral glucose load, that the glucose concentrations during the 2-hour period of these two tests are highly correlated. There is epidemiological evidence that the 2-hour post-load-glucose is more predictive of cardiovascular mortality than fasting glucose, but it would appear that they are equally predictive of retinopathy. While hyperglycaemia is related with cardiovascular mortality, clinical trials lowering glucose levels in type 2 diabetic patients, have not succeeded in reducing cardiovascular disease rates, in contrast to the beneficial effects on micro-vascular disease. STOP-NIDDM, a clinical trial testing the prevention of type 2 diabetes, used the glucose lowering agent acarbose, a drug which lowers postprandial glucose. There was a beneficial effect on cardiovascular outcomes, however, the number of events was extremely small and the study was not designed to test this effect. Confirmatory studies are required before it is possible to conclude that acarbose is effective in cardiovascular prevention, and that indeed it is the treatment of postprandial glucose which is beneficial. The cardiovascular disease in diabetic patients may be due to the presence of other cardiovascular risk factors associated with diabetes.
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PMID:Epidemiological data on postprandial glycaemia. 1737

Diabetes mellitus is a chronic disease caused by inherited and/or acquired deficiency in production of insulin by the pancreas, and by resistance to insulin's effects. Such a deficiency results in increased concentrations of glucose and other metabolites in the blood, which in turn damages many of the body's systems, in particular the eyes, kidneys, nerves, heart and blood vessels. There are two major types of diabetes mellitus: Type 1 diabetes (insulin-dependent diabetes, IDDM or juvenile onset diabetes) and Type 2 diabetes (non-insulin-dependent diabetes, NIDDM or adult-onset). Chronic hyperglycemia is a major initiator of diabetic micro- and cardiovascular complications, such as retinopathy, neuropathy and nephropathy. Several hyperglycemia-induced mechanisms may induce vascular dysfunctions, which include increased polyol pathway flux, altered cellular redox state, increased formation of diacylglycerol (DAG) and the subsequent activation of protein kinase C (PKC) isoforms and accelerated non-enzymatic formation of advanced glycated end products. It is likely that each of these mechanisms may contribute to the known pathophysiologic features of diabetic complications. Others and we have shown that activation of the DAG-PKC pathway is associated with many vascular abnormalities in the retinal, renal, neural and cardiovascular tissues in diabetes mellitus. DAG-PKC pathway affects cardiovascular function in many ways, such as the regulation of endothelial permeability, vasoconstriction, extracellular matrix (ECM) synthesis/turnover, cell growth, angiogenesis, cytokine activation and leucocyte adhesion, to name a few. Increased DAG levels and PKC activity, especially alpha, beta1/2 and delta isoforms in retina, aorta, heart, renal glomeruli and circulating macrophages have been reported in diabetes. Increased PKC activation have been associated with changes in blood flow, basement membrane thickening, extracellular matrix expansion, increases in vascular permeability, abnormal angiogenesis, excessive apoptosis and changes in enzymatic activity alterations such as Na(+)-K(+)-ATPase, cPLA(2), PI3Kinase and MAP kinase. Inhibition of PKC, especially the beta1/2 isoform has been reported to prevent or normalize many vascular abnormalities in the tissues described above. Clinical studies have shown that ruboxistaurin, a PKCbeta isoform selective inhibitor, normalize endothelial dysfunction, renal glomerular filtration rate and prevented loss of visual acuity in diabetic patients. Thus, PKC activation involving several isoforms is likely to be responsible for some of the pathologies in diabetic retinopathy, nephropathy and cardiovascular disease. PKC isoform selective inhibitors are likely new therapeutics, which can delay the onset or stop the progression of diabetic vascular disease with very little side effects.
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PMID:The role of protein kinase C activation and the vascular complications of diabetes. 1757 31

The present study was conducted to document the association between plasma homocysteine levels and the presence of macrovascular angiopathy with food and nutrient intake patterns among patients with Type II diabetes mellitus in Korea. Plasma total homocysteine concentration was analyzed by HPLC-fluorescence detector method in 127 patients with non-insulin dependent diabetes mellitus. Logistic regression analyses were performed respectively to study the association of plasma homocysteine levels with clinical and dietary characteristics and macroangiopathy (MA). The average plasma homocysteine level of patients with MA was 14.2 micromol/l, which was significantly higher than that of patients without MA (11.4 micromol/l). The proportions of patients with MA showed a significant difference, being 32.3% in hyperhomocysteinemic (>14.0 micromol/l) patients and 13.5% in others with homocysteine levels lower than 14.0 micromol/l. Odds ratios for macroangiopathy by tertile increase of plasma homocysteine concentration were 1.633 (Q(2)) and 4.831 (Q(3)), when adjusted for age, sex, and cigarette smoking. Patients with MA consumed reduced amounts of vitamin B(1), B(2), and folate. The results indicate that the plasma homocysteine levels are significantly increased in NIDDM patients who have macroangiopathy. Dietary management such as increased fruits and vegetables and decreased potatoes and starches might be beneficial for the prevention of macroangiopathy in diabetic patients.
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PMID:Plasma total homocysteine and macrovascular complications are associated with food and nutrient intake in patients with Type II diabetes mellitus. 2053 90


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