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

Diabetes affects the microcirculation, the large arteries and occasionally the large and small veins, by inducing vessel wall sclerosis. The degree of stiffening produced is linked to its duration. The ability of the diabetic's circulation to distribute blood is affected, especially during increased blood flow. In most tissues this causes no serious burden, but three tissues are unusually susceptible to disturbance--the retina, renal cortex, and peripheral nerve. They develop serious problems in many longstanding diabetics. Damage to the kidney appears to be linked to its unique combination of high blood flow rate and precise control of intraglomerular filtration pressure. As renal arteriolar intima hyalinizes, the glomerular mesangium increases in volume. Diabetic renal changes appear to become irreversible when a critical stage, manifested be albuminuria and hypertension, is reached. The resulting renal failure is associated with clumpy deposits of type IV collagen in the cortex, suggesting that local microvascular autoregulation has been lost. The retinal circulation forms late in fetal life in a process in which local oxygen tension controls new vessel formation. In adult diabetics, local retinal oxygenation is disrupted by a condition called capillary closure, and intraretinal microaneurysms form. In advanced retinopathy, new microvessel systems grow into the vitreous through defects in the internal limiting membrane, producing hemorrhage and vitreous opacification. Macular degeneration is also seen in older diabetics, suggesting that the choroidal circulation may also be compromised. Evidence for a microcirculatory role in diabetic peripheral nerve damage is not as conclusive as for the kidney and retina. The longest peripheral nerves are typically the most affected. Recent studies suggest that nerve damage can be produced by a disturbance in local pressure-flow relationships combined with epineurial mechanical constraint. Hypotheses about the pathogenesis of diabetic vascular sclerosis are reviewed, including collagen-stiffening, elastin degeneration, hemorheologic burden, metabolic disruption, increased permeability, and auto-immune disturbance.
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PMID:The microcirculation in diabetes. 640 Apr 26

Pressure-volume characteristics and morphologic changes were investigated in lungs of growing rats with streptozotocin-induced diabetes mellitus. Lung elastic recoil examined with quasi-static, air-filled pressure-volume curves showed no significant differences from that in control rats at all lung volumes. No alterations of surfactant properties as measured by a surface balance were observed. A 24% increase in the volume proportion of alveolar wall was found in the lungs from diabetic rats. There was an increase in the relative amounts of collagen, elastin, and basal laminae in the alveolar wall. There were more alveoli per unit volume in the diabetic animals (49.12 X 10(5)) than in the control animals (39.80 X 10(5)) (p less than 0.05) and there was an increase in the surface-to-volume ratio of the lungs of the diabetic rats.
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PMID:Changes in lung morphologic features and elasticity caused by streptozotocin-induced diabetes mellitus in growing rats. 668 63

The purpose of this paper is to review and to illustrate some of the themes underlying recent research on the aging of connective tissues. The systematic variation with age of the relative rates of biosynthesis (and of degradation) of the macromolecules of the intercellular matrix (collagens, elastin, proteoglycans and structural glycoproteins) is interpreted as the result of an "age program" of matrix synthesis by differentiated mesenchymal cells. This relative rates of synthesis of a well-defined set of matrix macromolecules can be used in its turn to define the state of differentiation (and of aging) of mesenchymal cells. This relative rate of synthesis of a well-defined set of matrix macromole-followed by its degradation through the elastases. The increasing frequency of some diseases with age ("aging diseases" of connective tissues, athero-/arteriosclerosis, diabetes, osteoarticular diseases, etc.) is probably related to this changing composition of the intercellular matrix. Cell-matrix interaction does depend on the secretion of a specific matrix which in its turn influences cell behaviour. With changing matrix composition (changing cell environment) cell behaviour will also change. This informational feedback mechanism may be of great importance in the aging of connective tissues and also in the increasing frequency of some pathologies with age.
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PMID:Aging of connective tissue. 690 13

Diabetes is generally accompanied by abnormal levels of growth hormone and adrenal steroids, hormones known to modulate postpneumonectomy (post-PNX) compensatory lung growth. Thus, we examined the possibility that diabetes may affect post-PNX lung growth processes. Left PNX was performed in young diabetic rats (streptozotocin-induced; 75 mg/kg body weight) (DM-PNX) and in control rats (C-PNX), for comparison with sham-operated control rats (C-SHAM). The rats were permitted free access to food and water. Examination at day 7 after surgery showed that right lung absolute dry weight and absolute DNA, collagen and elastin contents were increased in C-PNX and DM-PNX rats (but only C-PNX values reached those of both lungs in C-SHAM rats). Body weights (BW) of DM-PNX rats were lower than those of C-PNX and C-SHAM rats. Lung DNA/BW in C-PNX and DM-PNX rats were comparable, and matched values for both lungs in C-SHAM rats. Lung dry weight/BW, collagen/BW, and elastin/BW in DM-PNX rats exceeded values in C-PNX rats and even more for values of both lungs in C-SHAM rats. Data of another experiment, comparing DM-PNX rats with body weight-matched (by food limitation) PNX and control rats (WMC-PNX and WMC-SHAM rats, respectively) indicated comparable lung absolute DNA contents in DM-PNX and WMC-PNX rats (which matched values for both lungs in WMC-SHAM rats), however, lung absolute collagen and elastic contents were greater in the DM-PNX rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of streptozotocin-induced diabetes on postpneumonectomy lung growth and connective tissue levels. 756 17

Lipochondral degeneration (LCD) was found in the capsular tissue of 33 of 74 resected osteoarthritic hips studied retrospectively and in 14 of 35 studied prospectively, but never in a control group (n = 46). The process arose in the ligamentous structures that had undergone nodular chondroid metaplasia. The lesion was characterized by vacuolar distention of chondrocytes, eventual necrobiosis, and formation of acellular pools of lipid material. The latter was shown by oil red O staining and electron microscopy. Matrix alterations included glycosaminoglycan depletion, formation of elastin-related material, and degeneration of collagen fibers. There was no significant correlation (p = 0.05) between the occurrence of LCD and the severity of the osteoarthritis; neither was any association found with age, sex, calcium pyrophosphate dihydrate deposition, diabetes mellitus, or coronary artery disease.
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PMID:Lipochondral degeneration of capsular tissue in osteoarthritic hips. 787 26

The relationship between glycation of the aortic elastin and calcium deposits in the aorta was studied in streptozocin (STZ)-induced diabetic rats. 5-Hydroxymethylfurfural (5-HMF) which was released from aortic elastin by acid, was assayed after STZ treatment as an index of early stage glycation. The amount of released 5-HMF increased at 5 weeks and paradoxically decreased at 10 weeks after STZ treatment, though it remained higher than that of control rats. This paradoxical pattern was reproduced by the in vitro incubation of elastin with glucose and it is presumably due to further advancement of glycation reactions in diabetic rats. The level of 5-HMF did not change significantly in control rats at corresponding time points of 9, 11 and 16 weeks of age. Fluorescence of porcine pancreatic elastase I-digested elastin which served as an index of advanced glycation, increased by 1.6 times at 3 weeks and reached a maximum of 1.9-fold higher than that of control rats at 10 weeks. The calcium content of the aorta at 10 weeks in diabetic rats was significantly increased by 1.4-fold compared with control rats. This study showed that the increased elastin glycation in the aorta even at the early stage of diabetes is associated with calcium deposit in the aorta. These results are consistent with the interpretation that elastin glycation in the aorta is the potential accelerating factor for diabetic macroangiopathy.
Diabetes Res Clin Pract 1993 Jan
PMID:Association of elastin glycation and calcium deposit in diabetic rat aorta. 847 16

A novel amino acid named aldosine was isolated from acid hydrolysates of bovine aorta elastin. The mass spectral analysis of aldosine indicated a parent compound with a mass of 256 (C12H20N2O4). From the structure identified by spectroscopy of aldosine and its derivatives, it was deduced that aldosine was derived from aldol crosslink and dehydromerodesmosine of elastin and collagen. The aldosine content in aorta of newborn rats was very low, but increased markedly with growth. After maturity was reached, the aldosine content decreased. The aldosine content in bovine aorta decreased gradually from 7 months to 16 years of age. Aldosine was also quantified in the aorta and tail tendon of rats in two models of hyperglycemia: diabetes and galactosemia. Hyperglycemias were significantly affected on aldosine content of organs. In both diabetic and galactosemic animals, aldosine was remarkably lower relative to controls (about one-half and one-sixth, respectively).
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PMID:An amino acid derived from aldol crosslink of elastin and collagen: structure, distribution, aging, and two models of hyperglycemia. 856 94

The present study focuses on the differential response of three branch levels of the mesenteric resistance arterial vasculature of 450-gram Sprague-Dawley rats infused continuously with angiotensin II (A-II) for 4, 7 and 14 days at a rate of 435 ng/kg/min, with an associated period of hypertension. The three branch levels (types I, II and III) were characterized by light microscopy and immunostaining using monoclonal antibodies for proliferating cell nuclear antigen, ED-1 (specific for rat monocytes/macrophages) and alpha smooth muscle cell (SMC) actin. Cross-sectional areas of the vascular walls were determined morphometrically. In situ hybridizations were performed on paraffin sections using both sense and antisense 35S-labeled cRNA probes generated from rat SMC osteopontin and elastin cDNAs. In the type-I (penetrating) arteries from A-II-infused animals, there was massive fibrinoid necrosis, a marked fibroproliferative perivascular response, intense monocyte/macrophage infiltration, striking SMC osteopontin and elastin gene expression; SMC, fibroblast and monocyte/macrophage DNA synthesis; and significant increase in the cross-sectional areas of the vascular walls. In the same animals, DNA synthesis also occurred in the larger mesenteric arteries of types II and III where it is associated with significant enlargement of the walls by SMC hypertrophy but without overt morphologic damage. It is suggested that the monocyte/macrophage infiltration and fibroproliferative response of type-I arteries may be related to A-II-induced osteopontin gene expression. Angiotensin infusion in the rat may represent a reproducible model of microvascular injury that can be utilized to elucidate the cellular and molecular biology of a variety of disease states such as hypertension and diabetes mellitus.
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PMID:Immunohistochemical and molecular characterization of the differential response of the rat mesenteric microvasculature to angiotensin-II infusion. 892 18

The most serious late complication of ageing and diabetes mellitus follow similar patterns in the dysfunction of retinal capillaries, renal tissue, and the cardiovascular system. The changes are accelerated in diabetic patients owing to hyerglycaemia and are the major cause of premature morbidity and mortality. These tissues and their optimal functioning are dependent on the integrity of their supporting framework of collagen. It is the modification of the properties by glycation that results in many of the damaging late complications. Initially glycation affects the interactions of collagen with cells and other matrix components, but the most damaging effects are caused by the formation of glucose-mediated intermolecular cross-links. These cross-links decrease the critical flexibility and permeability of the tissues and reduce turnover. In contrast to the renal and retinal tissue, the cardiovascular system also contains a significant proportion of other fibrous connective tissue protein elastin, and its properties are similarly modified by glycation. The nature of these glycation cross-links is now being unravelled and this knowledge is crucial in any attempt to inhibit these deleterious glycation reactions.
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PMID:Glycation of collagen: the basis of its central role in the late complications of ageing and diabetes. 902 89

The relations of biological markers of extracellular matrix (plasma elastin peptides and elastase inhibitors) to the clinical history of cardiovascular diseases and risk factors for atherosclerosis were examined in a large population study (the EVA Study) on vascular and cognitive aging performed in 1389 men and women aged 59-71 years. A moderate decrease in elastin peptides was observed in women with a self-reported history of coronary heart disease (P < 0.091) and stroke (P < 0.03) as well as with diabetes (P < 0.043). Similar but non-significant trends were found in men. Furthermore, elastin peptides were significantly and positively correlated to HDL-cholesterol and apolipoprotein A1 in both sexes. On the other hand, elastase inhibitor titers were significantly higher in women than in men. A moderate increase was also found in men (P < 0.097) and women (P < 0.068) with a history of coronary heart disease that reached significance level after pooling both sexes (P < 0.014). Furthermore, elastase inhibitor titers were significantly and positively related to fibrinogen and C reactive protein in either sex. No consistent associations were observed between both biological markers of extracellular matrix and age, blood pressure, body mass index and tobacco or alcohol consumption. These results suggest that a decrease in elastin peptides and an increase in elastase inhibitors might be associated with risk factors of atherogenesis as well as with atherosclerosis-related diseases.
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PMID:Aging of the vascular wall: serum concentration of elastin peptides and elastase inhibitors in relation to cardiovascular risk factors. The EVA study. 918 Feb 47


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