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

Increased thromboxane A2 (TXA2) generation by platelets has been reported both in diabetic patients and streptozocin-induced diabetic rats. This increase is in contrast to the decreased prostacyclin (PGI2) synthesis by endothelial cells in diabetes. An imbalance in the ratio of TXA2/PGI2 has been implicated in increased platelet aggregation and a high incidence of vascular disease in human diabetes. The mechanism for this imbalance, however, remains elusive. In a previous study from our laboratory, we reported unchanged arachidonic acid levels in platelet membrane phospholipids of 3-week diabetic rats, but a decreased arachidonic acid level in platelet membrane phospholipids of 6-week diabetic rats. In the present communication, we report the role of enzymes that are involved in remodeling arachidonic acid levels of platelet membrane phospholipids in both 3- and 6-week diabetic rats. No alterations were observed in the activities of arachidonoyl-CoA synthetase, acyl-CoA: lysophosphatidylcholine acyltransferase, or phospholipase A2 in platelets from both 3- and 6-week diabetic rats. However, both increased uptake and incorporation of [14C]arachidonic acid into platelets were observed in the diabetic platelet-rich plasma. In conclusion, increased TXA2 formation in diabetic platelets is not due to alterations in the activities of enzymes involved in the incorporation into or release of arachidonate from the diabetic platelet membrane phospholipid, but may be due to increased efficiency of uptake, incorporation or possibly redistribution of this fatty acid among phospholipid classes in diabetic platelets.
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PMID:Modifications of platelet phospholipid fatty acid composition in streptozocin-induced diabetic rats. 143 63

Recent studies concerning secular trends in stroke incidence and mortality and identification of independent risk factors for stroke are reviewed. Stroke mortality has declined in many industrialized countries in recent decades. In France, it has been declining by more than 30% between 1968 and 1982 in all age groups and in both sexes except for women under 40 years. The decline in stroke mortality seems to be partly real and partly apparent. In the community-based study of Rochester, Minnesota, stroke incidence decreased by 54% between 1945-49 and 1975-79. Recent data from Rochester, however, suggest that the incidence of stroke may no longer be declining. Survival after stroke has also apparently been improving but several sources of potential bias may also have influenced the decrease in reported survival rates. Hypertension is a major risk factor for stroke. Prolonged differences in "usual" diastolic blood pressure of 5 to 10 mmHg are associated with about 40% difference in stroke incidence. Recent analysis suggests that stroke incidence reduction could arise rapidly after hypertension control and that a lower blood pressure should confer a lower risk of vascular disease, even in individuals conventionally considered as "normotensive". There is evidence that cigarette smoking is an important risk factor for stroke with an overall relative risk of 1.5 and that the risk of stroke declines rapidly after the cessation of smoking. A cardiac condition may be a marker for another risk factor or the primary substrate for cerebral embolism. In patients with atrial fibrillation, the risk of stroke is increased through both of these mechanisms. Diabetes mellitus, chronic alcohol consumption (> 3 drinks/day), and high fibrinogen levels are other independent risk factors for stroke. While high levels of cholesterol may be associated with ischemic stroke, an inverse association of the serum cholesterol with the occurrence of intracerebral hemorrhage in men has been reported. In patients with asymptomatic internal carotid stenosis, higher degrees of stenosis convey a higher risk of stroke. However, far from all these strokes are due to thromboembolism from an atheromatous plaque in the ipsilateral internal carotid artery. The relative risk of stroke during the first 5 years following a transient ischemic attack is 7 times that in persons without transient ischemic attack. More than a third of the subsequent strokes occur in a vascular territory different from that of the incident TIA. While the use of oral contraceptives may increase the relative risk of stroke, postmenopausal estrogen treatment may have a protective effect on the risk of vascular diseases.
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PMID:[Epidemiology of cerebrovascular accidents]. 143 51

Percutaneous transluminal renal angioplasty (PTRA) is generally considered of little benefit in the treatment of ostial renal artery stenosis. This report contains long-term follow-up (> 12 months in all patients; mean follow-up, 38 months) for 110 patients who underwent PTRA for treatment of ostial renal artery stenosis. There was no significant difference in patient benefit related to bilaterality or multiplicity of lesions treated or to renal function before angioplasty (P > .1). Although there was no statistically significant difference in benefit among groups of patients who received treatment, certain trends were apparent. The least benefit occurred in patients with insulin-dependent diabetes and those with symptoms or history of vascular disease in another organ system. Treatment of lesions with proportionately larger balloons did not result in greater benefit. Restenoses were redilated in 16 patients for whom initial treatment failed. Eleven of these were ostial restenoses. The ostial stenosis in one patient was redilated a second time. At the end of follow-up, primary, secondary, and tertiary clinical benefits were 48%, 57%, and 58%, respectively. This was not statistically different (P = .14) from a control group of 94 patients with nonostial stenoses who had 68% long-term benefit. The authors conclude that ostial renal artery stenosis is not a contraindication to PTRA, and balloon angioplasty can play an important role in blood pressure control in this patient population.
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PMID:Long-term results of angioplasty in 110 patients with renal artery stenosis. 144 23

A total of 1,265 patients with age-related diseases such as diabetes, arthritis, vascular disease and hypertension as well as 1,100 persons in diminished health without apparent disease, were treated with the metal chelator EDTA and antioxidants such as vitamin C, E, beta-carotene, selenium, zinc and chromium. Good results were observed in the majority of patients. This is encouraging for the initiation of controlled clinical trials.
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PMID:Antioxidant therapy in the aging process. 145 Jun 4

Platelets could contribute to vascular disease in diabetes through enhanced adherence to collagen exposed in injured vessels. Increased platelet adherence to collagen in diabetes could result from an alteration in platelets and/or platelet hypersensitivity to collagen that has been glycated to a greater extent. In this study, the adherence of platelets from diabetic or control subjects to glycated or nonglycated collagen coated onto glass surfaces was examined. Membrane fluidity of platelets was also determined, since decreased membrane fluidity associated with increased glycation of membrane proteins of platelets from diabetic subjects was shown in a previous study, and decreases in membrane fluidity have been shown by others to increase platelet adhesion. Thirteen diabetic subjects were compared with 13 age-and sex-matched control subjects. Collagen was glycated (9.7 nmol glucose/mg protein) by preincubation for 12 days in glucose-rich medium (500 mmol/L). A control solution of collagen incubated without glucose for the same time had 3.3 nmol glucose/mg protein. There were no differences in the adherence of platelets from diabetic and control subjects to nonglycated and glycated collagen-coated glass. The mean steady-state fluorescence polarization value (0.187 +/- 0.002) in 1.6-diphenyl-1,3,5-hexatriene-labeled platelets from diabetic subjects was significantly greater than in platelets from control subjects (0.174 +/- 0.002, p < 0.002); thus membrane fluidity in platelets from the group of diabetic subjects was decreased. The extent of glycation of membrane proteins from diabetic subjects (25.4 +/- 0.5 nmol glucose/mg protein) was significantly greater than from control subjects (20.2 +/- 0.4 nmol glucose/mg protein, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduced membrane fluidity and increased glycation of membrane proteins of platelets from diabetic subjects are not associated with increased platelet adherence to glycated collagen. 145 13

The development of laboratory techniques for the culturing of vascular endothelial and smooth-muscle cells during the 1970s, followed by the rapid advances in molecular and cell biology during the 1980s, provided the foundation for the identification of growth factor and cytokine networks involved in maintenance of the normal vasculature as well as participating in diverse pathologic processes involving blood vessels. Vascular cells can produce and respond to a vast array of biochemical messengers that control cell replication, differentiation, and many specific cell functions. Investigators are beginning to explore the changes in the patterns of messengers exchanged between the vascular cells and infiltrating leukocytes during the initiation and progression of atherosclerosis. A variety of in vitro and in vivo studies have indicated that growth factors and cytokines that mediate the critical processes of inflammation and wound healing also play a central role in vascular disease. Indeed, many view atherosclerosis as the result of excessive or prolonged chronic inflammation and wound healing in response to diverse injurious stimuli to cells of the vessel wall. Vascular injury may result from many varied and interacting forces, including nutritional and metabolic abnormalities such as hyperlipidemias or elevated homocysteine, mechanical forces associated with hypertension, exogenous toxins including those found in cigarette smoke, abnormally glycated proteins associated with diabetes mellitus, oxidatively modified lipids or proteins, and, possibly, viral infections. Ultimately, a greater understanding of the activated cytokine and growth factor networks within the vascular wall following injury and during atherogenesis will allow clinical scientists to identify steps susceptible to therapeutic intervention using recombinant cytokines, antibodies, soluble receptors, or receptor antagonists. Other therapeutic strategies may involve the transfection of specific genes, which may inhibit atherosclerosis, into vascular cells at sites prone to lesion formation.
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PMID:Cytokines and growth factors in atherogenesis. 145 74

Diabetes is accompanied by impaired platelet function and accelerated vascular disease. To find out whether a correlation exists between these two complications, and if modifications occurring in diabetic platelets influence their relationship with endothelium, we have studied the interaction between platelets isolated from plasma of diabetic patients and bovine valvular endothelial cells (VEC), in culture. For quantitative analysis, normal and diabetic [3H]-adenine-labeled platelets were incubated with confluent VEC grown in Dulbecco's modified Eagle medium, containing 4.5 g/l glucose, for 30 min at 37 degrees C. After extensive washing and solubilization of the monolayer, the calculated adhesion index showed a two-fold increased adherence of diabetic platelets to VEC as compared to normal platelets. Statistical analysis (by Pitman randomization test) indicated that the adhesion was significantly higher (p = 0.0003) than that of normal platelets to VEC. To partially identify the membrane components implicated in the adhesion process, either platelets or VEC were treated with neuraminidase, trypsin or heparinase prior to the adhesion assay. Trypsin or neuraminidase treatment of platelets significantly diminished their adherence to VEC, suggesting a role of platelets sialylated glycoproteins in the adhesion process. Neuraminidase or heparinase treatment of VEC increased the adhesion of both normal and diabetic platelets, indicating that the cell membrane sialyl residues and heparan sulfate participate in the normal thromboresistant properties of VEC. Transmission and scanning electron microscopy revealed a close apposition between platelets and VEC with the formation of an adhesion plaque, characterized by fine fibrillar bridges between the plasma membranes of the two cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased adhesion of human diabetic platelets to cultured valvular endothelial cells. 145 40

High density lipoprotein subfraction 2 (HDL1)-cholesterol level is usually decreased in Type 2 (non-insulin-dependent) diabetes. A study was carried out in 251 Type 2 diabetic patients (106 males [M], 145 females [F]) and in 120 non diabetic controls in order to determine the influence of hypertriglyceridaemia and obesity on the HDL2-cholesterol level and to analyse the relationship between HDL2-cholesterol level and atherosclerosis (coronary heart disease, peripheral atherosclerosis or cerebral vascular disease), in Type 2 diabetes. Influence of hypertriglyceridaemia and obesity on HDL2-cholesterol level was studied by comparing the mean values of HDL2-cholesterol between diabetics and controls, after controlling for hypertriglyceridaemia and obesity, and by a multiple linear regression test. A stepwise logistic regression was performed to analyse the association between the prevalence of atherosclerosis and several variables: age, duration of diabetes, hypertension, cigarette smoking, body mass index, mean glycaemia, total cholesterol, triglyceride, HDL-cholesterol, HDL2-cholesterol and HDL3-cholesterol levels. In both men and women, when both of the factors (hypertriglyceridaemia and obesity) were present of when only one was, HDL2-cholesterol level was significantly lower in the diabetic population, compared with controls. But when obesity and hypertriglyceridaemia were absent, HDL2-cholesterol level, in the diabetic population, was not significantly different from controls (M: 17.9 +/- 13.3 vs 20.5 +/- 13.8 mg/dl: NS; F: 30.1 +/- 21.5 vs 27.6 +/- 14.2 mg/dl: NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of obesity and hypertriglyceridaemia on the low HDL2-cholesterol level and on its relationship with prevalence of atherosclerosis in type 2 diabetes. 145 17

The natural history of peripheral arterial occlusive disease is discussed. Severe limb-threatening ischemia is the most serious consequence of chronic arterial occlusive disease. Severe ischemia and amputation can be considered as an endpoint in peripheral vascular disease. Severe limb ischemia is relatively uncommon in isolated aortoiliac disease and this is more than twice in patients with either femoropopliteal or multisegmental disease. Subsequent studies have also demonstrated that both smoking and diabetes are associated with a substantial risk for sudden ischemia. A clear majority of about 50% deaths are caused by associated coronary artery disease, 15% to stroke and 10% to vascular disease in the abdomen. Ankle systolic blood pressure is one of the most significant factors in the progression of peripheral arterial occlusive disease and also for cardiovascular mortality. In the future, men need to know how therapies as exercise, during regimens would influence the most frequent complications besides severe limb ischemia, namely brain infarction and coronary artery disease.
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PMID:Natural history and evolution of peripheral obstructive arterial disease. 146 Mar 49

Diabetic vascular disease is more severe, diffuse, and accelerated when compared to nondiabetic vascular disease. Endothelial cell injury or alteration in endothelial cell function is hypothesized to be the initial cellular event in the pathophysiology of diabetic vascular disease. We examined the effect of insulin-treated and untreated alloxan diabetes on the proliferation of rabbit aortic endothelial cells in vitro by growing thoracic aortic endothelial cells from alloxan diabetic rabbits in serum obtained from alloxan diabetic rabbits. Diabetes adversely affected the proliferation of aortic endothelial cells; the most significant decrease in cell proliferation was noted in untreated diabetic cells. Crossover studies between endothelial cells and serum from different groups revealed that diabetes slows endothelial proliferation by not only a serum effect but also an intrinsic cellular effect. These observations suggest that diabetes adversely affects the proliferation of aortic endothelial cells by changing cell and serum functions.
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PMID:The effect of diabetes on the proliferation of aortic endothelial cells. 146 63


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