Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was made of the level of fibronectin in 42 pediatric patients with insulin dependent diabetes mellitus. Blood plasma fibronectin was determined by an immunoturbidometric method. A raised concentration of fibronectin was established in patients with a period of disease over 5 yrs., in decompensation of 3rd degree, and the presence of microangiopathies.
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PMID:[The fibronectin level in children with diabetes mellitus]. 276 63

Diabetic microangiopathy may be associated with the pathogenesis and progression of autonomic and peripheral neuropathy. In 17 long-standing type I diabetic patients with peripheral and autonomic cardiovascular neuropathy, several hemorheological and hemostatic alterations were found compared to 13 matched type I patients without neuropathy. In particular, increased plasma von Willebrand factor antigen (p less than 0.001), fibronectin (p less than 0.001) and fibrinogen (p less than 0.001) levels were demonstrated in neuropathic in comparison with non-neuropathic diabetic patients. Moreover negative correlations between these parameters and both motor and sensitive conduction velocity of median, sural and peroneal nerves were observed in diabetic patients with neuropathy. Higher blood viscosity (p less than 0.05 at shear-rate of 450 and 225 s-1; p less than 0.01 at 90 s-1; p less than 0.001 at 4.5 and 2.25 s-1), plasma viscosity (p less than 0.001) and lower erythrocyte filtrability (p less than 0.001) were also found in neuropathic compared to non-neuropathic diabetics. Increased prevalence of retinopathy (p less than 0.01) and nephropathy (p less than 0.001) was finally reported in patients with autonomic and peripheral neuropathy. Microvascular disease may be involved in the development of neuropathy in long-term type I diabetes mellitus.
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PMID:Hemorheologic and hemostatic changes in long-standing insulin-dependent (type I) diabetic patients with peripheral and autonomic cardiovascular neuropathy. 323 50

Fibronectin plasma concentrations were determined in 28 children with type I diabetes mellitus and 22 healthy children. No statistically significant difference was observed between the fibronectin concentrations in diabetic and non-diabetic children. Even in children with poor glycaemic control the fibronectin concentrations (glycosylated haemoglobin greater than 10%) were not significantly higher.
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PMID:Fibronectin in children with diabetes mellitus. 649 38

Although increased plasma fibronectin (PF) levels have been found in diabetic patients with microalbuminuria, there is still controversy about its clinical implication for detecting early diabetic nephropathy. To evaluate the PF concentration as a possible marker for early diabetic nephropathy, three groups of sex-and age-matched patients were studied I) 22 insulin dependent diabetic (IDDM) patients with microalbuminuria (mean age +/- SEM: 23.3 +/- 3.6 years, mean urinary albumin excretion rate (AER) +/- SEM: 47.1 +/- 39.5 micrograms/min); II) 17 IDDM patients with normoalbuminuria (mean age: 23.4 +/- 4.4 years, mean AER: 7.8 +/- 2.1 micrograms/min) and III) 20 healthy control subjects (mean age: 22.6 +/- 4.1 years, mean AER: 6.7 +/- 2.1 micrograms/min). PF and urinary excretion of albumin were measured by an immunoturbidimetric method using commercially available kits (Boehringer Mannheim GMBH FRG, and Miles Lab., UK). The mean PF was significantly higher in the group with microalbuminuria (406.5 +/- 122.9 micrograms/ml) than in the group with normoalbuminuria (295.6 +/- 96.9 micrograms/ml, P < 0.01) or in the control group (299.54 +/- 105.5 micrograms/ml, P < 0.01). A weak positive correlation was found between PF and urinary albumin values (r = 0.35, P < 0.05). There were no significant correlations between PF and the other variables such as age, duration of diabetes, body mass index, arterial blood pressure, fasting blood glucose, fructosamine and HbA1 in the diabetic patients or in the control group. Our results suggest that the PF concentration could be a weak marker for early diabetic nephropathy. We cannot therefore use PF instead of microalbuminuria because there is only a weak correlation between PF and microalbuminuria.
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PMID:Can we use plasma fibronectin levels as a marker for early diabetic nephropathy. 762 76

Activation of protein kinase C (PKC) is implicated as an important mechanism by which diabetes causes vascular complications. We have recently shown that a PKC beta inhibitor ameliorates not only early diabetes-induced glomerular dysfunction such as glomerular hyperfiltration and albuminuria, but also overexpression of glomerular mRNA for transforming growth factor beta1 (TGF-beta1) and extracellular matrix (ECM) proteins in streptozotocin-induced diabetic rats, a model for type 1 diabetes. In this study, we examined the long-term effects of a PKC beta inhibitor on glomerular histology as well as on biochemical and functional abnormalities in glomeruli of db/db mice, a model for type 2 diabetes. Administration of a PKC beta inhibitor reduced urinary albumin excretion rates and inhibited glomerular PKC activation in diabetic db/db mice. Administration of a PKC beta inhibitor also prevented the mesangial expansion observed in diabetic db/db mice, possibly through attenuation of glomerular expression of TGF-beta and ECM proteins such as fibronectin and type IV collagen. These findings provide the first in vivo evidence that the long-term inhibition of PKC activation in the renal glomeruli can ameliorate glomerular pathologies in diabetic state, and thus suggest that a PKC beta inhibitor might be an useful therapeutic strategy for the treatment of diabetic nephropathy.
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PMID:Amelioration of accelerated diabetic mesangial expansion by treatment with a PKC beta inhibitor in diabetic db/db mice, a rodent model for type 2 diabetes. 1069 58

Fibronectin is a family of glycoproteins that are present on many cell surfaces, in extracellular matrix and in plasma. Fibronectin might play an important role in pathogenesis of chronic diabetic complications. The aim of this study was to estimate plasma concentration of fibronectin in patients with recently onset and with long duration of type 1 diabetes mellitus. Moreover, the correlation between fibronectin concentration and HbA1c, duration of diabetes and late diabetic complications was assessed. The study was performed in 18 patients with recently onset of diabetes (aged 23.8 +/- 5.3 years, HbA1c 10.63 +/- 0.83%) (group A) and 21 patients with long history of diabetes (aged 33.9 +/- 10.5 years, mean diabetes duration 9.8 +/- 5.8 years, HbA1c 9.24 +/- 2.48%) (group B). The plasma concentration of fibronectin was estimated with the use of the ELISA test. The plasma fibronectin concentration was significantly higher in type 1 diabetic patients in comparison with healthy subjects (381.00 +/- 27.42 and 297.50 +/- 25.32 micrograms/ml, respectively, p < 0.05). The values observed in the patients with recently onset and long duration of diabetes and in the subjects with and without diabetic complications did not differ significantly (p > 0.05, p > 0.05). We noticed positive correlation between fibronectin concentration and HbA1c (r = 0.35; p < 0.05) and negative correlation with patients age (r = -0.35; p < 0.05). The results of our study suggest, that plasma fibronectin concentration in diabetes is increased independently from microangiopathy but rather results from hyperglycaemia.
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PMID:[Assessment of plasma fibronectin concentration in type 1 diabetic patients]. 1094 84

Fibronectins are adhesive proteins considered as markers of endothelial activation. Plasma fibronectin levels in diabetes mellitus (DM) have been found to be associated with atherosclerotic risk factors. This study was carried out to investigate plasma fibronectin and its relation with serum lipids, apolipoproteins AI, B100 and lp(a) in diabetic children. 35 children (19F/16M) with type I DM and 30 non-diabetic age and gender-matched controls were enrolled. Apolipoprotein and fibronectin concentrations were determined with nephelometric methods. Plasma fibronectin levels of the children with type I DM and the control group are not statistically different. HbA1c and triglycerides concentration are found to be significant predictors of plasma fibronectin in diabetic children, while effect of plasma cholesterol, apolipoprotein AI, B100 and lp(a) are insignificant. Diabetic children with triglycerides 1.13 mmol/l have elevated plasma fibronectin (median, 25th-75th percentiles; 29.6, 8.3-40.8 mg/dL) compared to the diabetic > or = 19.9, 8.6-30.7 mg/dL, p < 0.05) and non-diabetic children (16.6, 12.7-32.4 mg/dL, p < 0.01) with triglycerides < 1.13 mmol/L. On the other hand plasma fibronectin concentrations of diabetic and non-diabetic children with high triglycerides are not significantly different. In conclusion our data does not support the concept that plasma fibronectin is elevated in type I diabetes mellitus at least in children, but high plasma triglycerides secondary to diabetes or not is associated with higher FNp concentrations which may have implications on atherogenesis. Plasma cholesterol, apolipoproteins AI, B100 and lp(a) are not significant determinants of FNp in type I diabetic children.
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PMID:Triglycerides predict plasma fibronectin in children with type I diabetes mellitus rather than diabetes. 1214 10

Heart failure is known to be a complication of insulin-dependent (IDDM) and noninsulin-dependent diabetes mellitus (NIDDM) even in the absence of coronary heart disease or hypertension. The mechanisms leading to diabetic cardiomyopathy are unknown. The aim of the study was to characterize structural and functional alterations in hyperinsulinemic Zucker diabetic fatty (ZDF) rats treated with or without insulin. Diabetic animals showed a twofold increase in cardiomyocyte volume with increased left ventricular ANP but not BNP mRNA levels in spite of a reduced plasma renin activity (PRA) 2 months after onset of diabetes compared to nondiabetic littermates. These changes were associated with an increase in left ventricular performance as assessed by echocardiography. Insulin treatment led to a significant increase in body weight (BW), total heart weight, myocardial protein content, and left ventricular mass (LVM). Perivascular fibrosis and laminin thickness were significantly augmented in diabetic rat myocardium irrespective of insulin treatment, whereas interstitial collagen I and fibronectin were similarly found in diabetic and control myocardium. Initial stages of diabetic cardiomyopathy in hyperinsulinemic rats are characterized by cardiomyocyte hypertrophy and enhanced cardiac contractility. It is suggested that hyperinsulinemia may be involved in cardiac hypertrophy.
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PMID:Myocardial hypertrophy and enhanced left ventricular contractility in Zucker diabetic fatty rats. 1476 80

Type I diabetes mellitus is caused by an autoimmune destruction of the insulin-producing beta cells. The major obstacle in using transplantation for curing the disease is the limited source of insulin-producing cells. The isolation of human embryonic stem (hES) cells introduced a new prospect for obtaining a sufficient number of beta cells for transplantation. We present here a method for forming immature islet-like clusters of insulin-producing cells derived from hES cells. The protocol consisted of several steps. Embryoid bodies were first cultured and plated in insulin-transferrin-selenium-fibronectin medium, followed by medium supplemented with N2, B27, and basic fibroblast growth factor (bFGF). Next, the glucose concentration in the medium was lowered, bFGF was withdrawn, and nicotinamide was added. Dissociating the cells and growing them in suspension resulted in the formation of clusters which exhibited higher insulin secretion and had longer durability than cells grown as monolayers. Reverse transcription-polymerase chain reaction detected an enhanced expression of pancreatic genes in the differentiated cells. Immunofluorescence and in situ hybridization analyses revealed a high percentage of insulin-expressing cells in the clusters. In addition to insulin, most cells also coexpressed glucagon or somatostatin, indicating a similarity to immature pancreatic cells. Further improvement of this insulin-producing cell protocol may lead to the formation of an unlimited source of cells suitable for transplantation.
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PMID:Differentiation of human embryonic stem cells into insulin-producing clusters. 1515 4

BACKGROUND: Latent tissue scurvy in clinical and experimental ascorbic acid (AA) deficiency resembles diabetic microangiopathy as reflected in capillary hyperperfusion and increased transcapillary escape rate (TER), von Willebrand factor (vWf), and capillary fragility (CF). We aimed to investigate the possible clinical impact of the low plasma AA level observed in type 1 diabetes mellitus. METHODS: Twenty normoalbuminuric patients with retinopathy were included in a randomized, double-blinded, placebo-controlled 6-month study with AA (6 g/day; n=10, mean age+/-S.D. 35.3+/-8.5 years, diabetes duration 17.2+/-3.3 years) or placebo (n=10; mean age 37.8+/-6.6 years, diabetes duration 18.4+/-1.7 years). RESULTS: An inverse correlation between log plasma AA (HPLC method) and TER of (125)I-labelled albumin was found (r=-0.66, p=0.002). TER decreased in the AA-treated group from 6.8+/-1.0 to 5.4+/-1.5%/h compared to the unchanged placebo group (from 5.6+/-1.5 to 5.9+/-1.1%/h; p=0.031). The CF (capillary resistance test) decreased in the AA group compared to the placebo group (p=0.028), while vWf, fibrinogen and fibronectin levels, and glomerular filtration rate (clearance of (125)I-iothalamate) remained unchanged. CONCLUSIONS: The results suggest that a low plasma AA level might be associated (pathogenetic?) with development of microangiopathy in type 1 diabetes mellitus and points to a possible treatment modality.
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PMID:Vitamin C treatment reduces transcapillary escape rate of albumin in type 1 diabetes. 1558 46


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