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

Microangiopathy is a systemic complication of diabetes that is especially severe in the retinal microcirculation. The objective of this study was to compare glucose uptake and glucose transporter expression between retinal endothelial cells and the closely related endothelial cells derived from the cerebral microcirculation. Endothelial cells isolated from bovine brain, bovine retinal, and rat heart microvessels were cultured in the presence of control (5 mM) and high levels of (30 mM) d-glucose for 1-5 days. Glucose uptake by cultured endothelial cells was determined by measuring the uptake of [(3)H]deoxy-d-glucose and glucose transporter protein expression was assessed by Western blot. Our results showed that glucose uptake was significantly (P < 0.001) higher in brain- and heart-derived endothelial cells than in retinal endothelial cells at both physiologic and high concentrations of glucose. High levels of glucose caused a significant (P < 0.05) decrease in glucose uptake in brain-derived and heart endothelial cells but had no effect on retinal endothelial cells. Similarly, in response to high glucose levels there was a significant (P < 0.01) down regulation of GLUT-1 in brain-derived endothelial cells but not in retinal endothelial cells. These results suggest that despite a low basal level of glucose uptake the inability of retinal endothelial cells to down regulate glucose uptake in the presence of high glucose levels could make them especially sensitive to the deleterious effects of hyperglycemia in diabetes.
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PMID:Differential glucose uptake in retina- and brain-derived endothelial cells. 1167 26

Patient with diabetes mellitus is prone develop vascular lesion of blood vessels of all kinds. Microangiopathy and atherosclerosis are progressive during the illness. Following the study of Stanley I. Rapport the at all scientist on blood brain barrier permeability change in experimental conditions, also with this study blood brain barrier change in the diabetes mellitus patients was observed. In patients with diabetes mellitus the level total proteins increased in the cerebrospinal fluid.
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PMID:[Permeability of the hematoencephalic barrier by proteins in diabetes mellitus]. 1191 94

Osteoporosis is well documented in type I diabetes, but its occurrence is controversial in type II diabetes. Microangiopathy is a major complication of type I and type II diabetes. We studied bone and microvascular changes in the Cohen diabetic rat, a unique nonobese model of noninsulin-dependent diabetes mellitus. The aim of this study was to find whether there is a temporal correlation between the onset of these two complications. The diabetic rats were divided into three groups (A, B, and C) according to duration of diabetes (2 months, 3 months, and 7 to 8 months, respectively). Trabecular bone area was assessed by computerized image analysis and microangiopathy by means of renal function tests, histologic examination of the kidneys, and ultrastructural measurement of the width of capillary basement membranes. Bone density of the distal femur and vertebra was significantly reduced in the diabetic rats relative to the control rats in all three groups (Group A femur: 11.5 +/- 1.6% versus 21.8 +/- 3.0%, p < 0.02; Group A vertebra: 15.9 +/- 1.6% versus 28.5 +/- 2.0%, p < 0.02; Group C femur: 7.9 +/- 1.1% versus 29.6 +/- 3.5%, p < 0.001; Group C vertebra: 11.4 +/- 0.7% versus 37.1 +/- 1.9%, p < 0.002). Renal function tests were normal in the Group A diabetic rats and there was marked albuminuria in the Group C diabetic rats. Histologic changes in the kidneys were seen only in the Group C diabetic rats. Five of 15 Group C diabetic rats showed no albuminuria or histologic evidence of kidney damage. The bone density in this subgroup was reduced relative to controls to the same degree as that of the rats with renal damage. There was no evidence of capillary basement membrane thickening in the Group A diabetic rats. Our findings indicate that in the Cohen diabetic rat, osteoporosis precedes the onset of microangiopathy. Microangiopathy probably does not play an important role in the pathogenesis of osteoporosis in this animal model.
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PMID:Osteoporosis in the Cohen diabetic rat: correlation between histomorphometric changes in bone and microangiopathy. 1237 74

The existence of a diabetic cardiomyopathy has been proposed as evidence has accumulated for the presence of myocardial dysfunction in diabetic patients in the absence of ischemic, valvular or hypertensive heart disease. Diastolic dysfunction has been described as an early sign of this diabetic heart muscle disease preceding the systolic damage. Abnormalities in diastolic performance have been first demonstrated by cardiac catheterisation and subsequently by mainly using echocardiography. The pathogenesis of this left ventricular dysfunction is not clearly understood. Microangiopathy, increased extracellular collagen deposition, or abnormalities in calcium transport alone or in combination are considered to be associated with this dysfunction. The relationship between diastolic dysfunction and glycemic control is still a matter of debate. Some epidemiological and clinical arguments suggest that diastolic abnormalities may contribute to the high morbidity and mortality among diabetic patients. However, the prognostic importance of subclinical diastolic dysfunction and the possibilities for intervention are not fully known. Eventually, despite numerous studies, evidence of an intrinsic diastolic dysfunction in diabetes mellitus remains questionable. Indeed, quite contradictory results have been reported. They have been obtained in small, inhomogeneous populations, with sometimes confounding factors, using various echocardiographic indices with known limitations. Also, further studies using more refined techniques for the evaluation of diastolic function are needed, as a prerequisite, to unequivocally relate diabetes mellitus to a specific cardiomyopathy.
Diabetes Metab 2003 Nov
PMID:Left ventricular diastolic dysfunction: an early sign of diabetic cardiomyopathy? 1463 22

Diabetes mellitus leads to several recognizable clinicopathologic neuropathic syndromes. Diagnosis and evaluation requires a thorough history and neurologic examination, electrophysiologic studies, blood studies and, in selected cases, cerebrospinal fluid analysis and nerve and muscle biopsy. Microangiopathy is the leading cause of diabetic neuropathy associated with metabolic, vascular ischemic and immunologic injury. Tight glycemic control and symptomatic therapy is beneficial in a minority of patients but does not prevent the relentless progression of symptoms and signs. Intravenous immune globulin is a novel therapy in patients with mononeuropathy multiplex, primary demyelinating neuropathy and peripheral nerve T-cells microvasculitis associated with C5b-9 membrane attack complex protein deposits.
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PMID:Diabetic peripheral neuropathy. 1498 76

Patient with diabetes mellitus is prone to develop the vascular lesion of blood vessels of all kinds. Microangiopathy and atherosclerosis are progressive during the illness. Also with this study blood brain barrier change in the diabetes mellitus patients was observed. In patients with diabetes mellitus the level of glucose and total proteins increased in the cerebrospinal fluid. During diabetes mellitus the change of permeability blood brain barrier is evident. Blood brain barrier permeability changes in the patients with ICV as well as in the patients without ICV correlate with the values of diabetes mellitus in blood.
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PMID:[Correlation between levels of blood glucose and cerebrospinal fluid glucose and proteins in diabetes mellitus]. 1501 1

Insulin deficiency induces an increase in blood glucose levels that, in long run, becomes toxic for many organs and systems. Microangiopathy and derangements in the immune function are known consequences of hyperglycemia, but the way in which these systemic alterations may affect pulmonary function has been scarcely investigated. Although confirmation from large clinical trials is still to come, the diabetic disease seems to hit the pulmonary microcirculation as any other organ by increasing vessel wall thickness and impairing gas exchange, which leads to a measurable loss of function and respiratory efficiency. In addition, a diabetic lung is more susceptible to low respiratory tract infections by atypical microorganisms and more likely to host severe episodes of pneumonia than a normal, non-diabetic lung. This is a review of current knowledge on the impact of diabetes mellitus in lung health. We have paid special attention to the role of metabolic control in preventing damage to the lung by sustained hyperglycemia.
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PMID:Pulmonary complications in diabetes mellitus: the role of glycemic control. 1558 94

Diabetic eye disease is the major cause of blindness and vision loss among working-age people in developed countries. Microangiopathy and capillary occlusion underlie the pathogenesis of disease. While laser treatment is regarded as the standard therapy, intensive medical management of glycaemia and hypertension is also a priority in order to reduce the risk of diabetic retinopathy. Recent data have prompted a re-evaluation of the role of lipid-modifying therapy in reducing diabetic retinopathy. The Fenofibrate Intervention for Event Lowering in Diabetes (FIELD) study demonstrated a significant 30% relative reduction in the need for first retinal laser therapy in patients with (predominantly early-stage) type 2 diabetes treated with fenofibrate 200 mg daily, from 5.2% with placebo to 3.6% with fenofibrate, p=0.0003. The benefit of fenofibrate was evident within the first year of treatment. These promising data justify further evaluation of the mechanism and role of fenofibrate, in addition to standard therapy, in the management of diabetic retinopathy.
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PMID:Diabetic retinopathy: treatment and prevention. 1793 59

The article presents the review of literature related to the analysis of current theories of the development of complicated I type diabetes mellitus in children. Special attention is given to the mechanisms of formation of late complications and in particular diabetic neuropathies. It is underlined, that the most important in pathogenesis of diabetic involvement of the nervous system is metabolic disorders, oxidizing stress, autoimmune processes. Microangiopathy plays certain role in formation of diabetic neuropathies, leading to disorders of microcirculation and hypoxia of nerves.
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PMID:[Clinical and pathogenetic mechanisms of the formation of complicated course of I type diabetes mellitus in children]. 1827 Nov 77

Red blood cell (RBC) adhesion to endothelium is increased in diabetes mellitus and is correlated with the severity of vascular complications. Microangiopathy is the most frequent complications in patients suffering from diabetes mellitus. Elevated glucose concentration increases the oxidation phenomenon and advanced glycation end product (AGE) formation. Plasma proteins, structural proteins and also RBC proteins can be glycated such as glycated hemoglobin and RBC membrane proteins. Interaction of plasmatic AGE or RBC bearing AGE with the receptor for AGE (RAGE) alters vascular function leading to a vascular hyperpermeability inflammatory reaction including oxidant stress and cytokine production. Reactive oxygen species (ROS) react with nitric oxide (NO) limiting its vasodilatory effect and NO synthase function is altered. All these factors may be at the origin of high blood pressure which is deleterious for the eye and kidney vasculature. AGE can act directly on vascular function but also through RAGE. AGE binding to RAGE alters endothelial cell function stimulating NADPH oxidase and reactive oxygen species production. Limiting oxidation, reducing AGE formation or interaction with RAGE is achievable by drugs already used for hypertension or diabetes, but new treatment by NO modulators may limit the deleterious effect of RBC adhesion to endothelium.
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PMID:Red blood cell adhesion in diabetes mellitus is mediated by advanced glycation end product receptor and is modulated by nitric oxide. 1925 29


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