Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study examined the association between urinary markers of early diabetic nephropathy and non-renal diabetic complications in 946 patients with type 2 diabetes mellitus. The association with hypertension was also studied. Data on macrovascular complications (ischaemic heart disease, stroke, peripheral vascular disease) and microvascular complications (retinopathy, peripheral neuropathy) were obtained from case records and clinical examination. Urine samples collected were analysed for albumin, beta(2)-microglobulin, retinol-binding protein (RBP), and N-acetyl-beta-D-glucosaminidase (NAG). Results showed that urinary albumin, RBP and beta(2)-microglobulin levels were higher in patients with macro- and/or microvascular complications, compared to those without. NAG levels were higher only in patients with both types of complications. A higher proportion of patients with complications had abnormally raised urinary protein and enzyme levels, compared to those without. Patients with associated hypertension had higher urinary levels of albumin and beta(2)-microglobulin, regardless of whether complications were present or not. RBP excretion was, however, markedly higher only in patients with microvascular complications, whereas hypertension did not influence NAG excretion. Urine albumin and RBP excretion were predictive of microvascular, as well as both macrovascular and microvascular complications, whereas NAG excretion was predictive of macro- and microvascular complications. These findings could mean that increased urinary protein and enzyme excretion were associated with more severe disease in these patients.
J Diabetes Complications
PMID:Urinary protein excretion in Type 2 diabetes with complications. 1111 88

The essential arterial hypertension is the second (after diabetes mellitus) cause of chronic renal failure which means a great social and economic burden to the society. It is well known that hypertension is a metabolic syndrome resulting in tissue injury. We tried to investigate the possible influence of some metabolic disturbances on renal function in nontreated essential hypertension. We have compared 25 patients with nontreated essential hypertension (11 women, 14 men) with 14 healthy volunteers (7 women, 7 men) matched for age. The patients' group was characterized by significantly higher urine excretion of NAG (N-acetyl-beta-D-glucosaminidase) (2.75 +/- 1.69 vs 1.82 +/- 1.46 p < 0.05) and a tendency to significantly higher urine fractional sodium excretion without significant difference in albumin excretion. These findings suggest that the tubular damage is present. We noticed the negative linear correlation between mean arterial pressure and (MAP) and NAG urine excretion in the group of hypertensive patients which may reflect the renal ischemia in tubulo-interstitial pathology. Our data suggests that in nontreated arterial hypertension the renal blood flow disturbances are the important cause of the deterioration of tubular function (which are earlier to glomerular damage).
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PMID:[Does any relationship exist between metabolic disturbances and some markers of renal damage in patients with untreated essential hypertension?]. 1139 62

The aim of this study was to establish and quantify changes in the activities of total, free and bound fractions of pancreatic lipase, galactoso-6-sulphatase, beta-D-galactosidase and N-acetyl-beta-D-glucosaminidase in the course of alloxan-induced diabetes mellitus. Rabbits were divided into a control group and groups injected with alloxan on the 21st, 42nd, 90th and the 180th day, after which blood samples were taken and the rabbits sacrificed by decapitation. The pancreas was removed and the glucose level measured. Enzyme activities were assayed by spectrophotometric methods. The total activities of N-acetyl-beta-D-glucosaminidase and beta-D-galactosidase were the lowest on day 42 of the test, and the total activity of lipase was the highest at this point of time, as compared to the other periods of the study. We conclude that in the course of alloxan-induce diabetes activities of pancreatic lipase and sulphatase were increasing following the levels of glucose, whilst activities of beta-D-galactosidase and N-acetyl-beta-D-glucosaminidase were declining, being inversely correlated to the level of glucose and activities of the first two mentioned enzymes. Above alterations in activity of lysosomal pancreatic enzymes of alloxan induced diabetic rabbits may be responsible for some aspects of previously reported diabetic enteropathy and chronic complications, or may provide a mechanism for the pancreatic beta-cells to moderate their insulin content.
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PMID:Changes in pancreatic lysosomal enzymes activity as the potential factors leading to diabetic enteropathy. 1178 76

Studies using pharmacologic inhibitors have implicated the enzyme aldose reductase in the pathogenesis of albuminuria and diabetic renal disease. However, a clear conclusion is not easily drawn from such studies since these pharmacologic inhibitors have nonspecific properties. To examine further the role of aldose reductase, we have overexpressed the human enzyme in a transgenic rat model. Transgene expression in the kidney was predominantly localized to the outer stripe of the outer medulla, compatible with the histotopography of the straight (S3) proximal tubule. The effect of enzyme overexpression on diabetes-induced renal function and structure was then investigated. Contrary to what may have been anticipated from the previous enzyme inhibition studies, diabetes-induced albuminuria was completely prevented by the overexpression of aldose reductase. No effect of overexpression of aldose reductase on renal structure nor on urinary excretion of beta2-microglobulin and N-acetyl-beta-D-glucosaminidase was observed in this transgenic rat model. In conclusion, our study strongly suggests that multiple roles for aldose reductase may give it a more complex place in diabetic nephropathy than is currently recognized.
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PMID:Prevention of diabetes-induced albuminuria in transgenic rats overexpressing human aldose reductase. 1216 24

In this follow-up study, 526 persons were followed for almost 5 years to assess the reversibility and predictive value of four kidney biomarkers in a field epidemiology setting. This study examined (a) whether elevations in urinary albumin, N-acetyl-beta-D-glucosaminidase, retinol-binding protein, and alanine aminopeptidase remained elevated at follow-up and (b) whether these initial elevations were predictive of kidney disease (as measured by markers of kidney dysfunction: serum creatinine, serum cystatin C, creatinine clearance, and urine osmolality) at follow-up. Study participants were 8-76 years of age at baseline and were followed for an average of 4.5 years. Approximately 50% of adults who had an elevated biomarker did not have an elevation at followup. Youths with elevated biomarkers at baseline, but who completed adolescence by the time of the follow-up, no longer had any elevations in biomarkers at follow-up. Adult participants who had elevated biomarkers and selected health conditions at baseline (diabetes and, to a lesser extent, heart disease, hypertension, gout, and urinary tract disease) were more likely to show early indicators of kidney impairment at follow-up. Participants with these health conditions and normal kidney biomarker values at baseline had kidney test results at follow-up that were similar to results of study participants who did not have these health conditions at baseline. The presence or absence of elevated biomarkers at baseline among generally healthy participants was not associated with the development of early indicators of kidney impairment at follow-up. This longitudinal study confirmed the utility of these four kidney biomarker tests as markers of preclinical organ dysfunction among adults with certain preexisting medical conditions.
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PMID:Confirming the utility of four kidney biomarker tests in a longitudinal follow-up study. 1457 88

Stefin A is the low-molecular, intracellular inhibitor of the human lysosomal cysteine proteinases, cathepsins B, H and L. The concentration of this inhibitor in plasma and in other biological fluids shows not only local expression and secretion but also immunity of the whole organism. The aim of our study was to examine if concentration of stefin A in plasma of patients with diabetes type 2 is different than in healthy subjects, depends on vascular complications, body mass index, glycaemic control and whether exists the relationship between activities of cathepsin B (CB) as well as N-acetyl-beta-D-glucosaminidase (NAG). In plasma of 62 diabetic patients and 14 control subjects, concentration of stefin A (using ELISA test) and activities of CB and NAG (using fluorescence methods) were investigated. Concentration of stefin A (4.95 micrograms/l) in comparison to control (2.80 micrograms/l) increased statistically significantly (p < 0.05). The highest increase of stefin A was discovered in patients with macrovascular complication (7.70 micrograms/l) and was significantly different (p < 0.01) in comparison with control group and patients with microangiopathy as well as both types of complications (micro- and macroangiopathy). Significantly higher concentration of stefin A was noted in patients with overweight and obesity (5.50 micrograms/l and 6.05 micrograms/l). No influence of glycaemic short and long term control on concentration of this inhibitor was observed. In patients divided into subgroups according to increasing plasma NAG activity, increase of stefin A was noted successively from subgroup K2 to K4 (NAG from 8.80 U/l to above 12.82 U/l). The results indicate contribution of stefin A in pathogenesis of vascular complications in patients with diabetes type 2 and its relationship with obesity.
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PMID:[Serum stefin A in patients with type 2 diabetes]. 1523 Feb 13

We investigated urinary N-acetyl-beta-D-glucosaminidase (NAG) levels in children with type 1 diabetes as an early marker of tubular damage and studied its correlation with microalbuminuria and glycaemic control. The study group comprised 42 children with type 1 diabetes and 20 healthy children as control. Urinary NAG to urinary creatinine ratio, microalbuminuria, glycated haemoglobin (Hb A1c), blood urea and serum creatinine were estimated. Urinary NAG levels in the children with diabetes were significantly higher than those of controls. There were positive correlations between urinary NAG levels and microalbuminuria, Hb A1c and systolic and diastolic blood pressure values. We found that 59.5% of diabetic children were positive for urinary NAG, while 38.1% of them were positive for microalbuminuria.
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PMID:Urinary N-acetyl-beta-D-glucosaminidase in children with diabetes as an early marker of diabetic nephropathy. 1533 May 57

Disturbed metabolism of glycosaminoglycans (GAGs) has been proposed to play an important role in the pathogenesis of late diabetic complications. The effect of diabetic complications and metabolic control on both total serum GAGs content and the serum activity of lysosomal glycosidases (N-acetyl-beta-D-glucosaminidase, alpha-L-fucosidase, beta-D-galactosidase, and alpha-D-mannosidase) contributing to GAGs degradation, was investigated in 48 patients with type 2 diabetes mellitus. The activity of beta-D-glucosidase and acid phosphatase, the lysosomal enzymes unrelated to GAGs metabolism, was determined for comparison. The elevated serum total GAG concentration in diabetic patients was strongly and positively influenced by poor metabolic compensation of diabetes and the presence of vascular complications. A similar tendency has been shown in regard to the activity of enzymes involved in GAG degradation, especially N-acetyl-beta-D-glucosaminidase, alpha-L-fucosidase and beta-D-galactosidase. Furthermore, the total serum GAG concentrations, as well as the activity of lysosomal enzymes involved in the extracellular matrix degradation, closely followed metabolic compensation, regardless of diabetic vascular complications. Thus, we suggest that increased values of the investigated parameters may indicate the degree of endothelial cell dysfunction and may be useful to predict the development of diabetic vascular pathology.
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PMID:Alterations of glycosaminoglycan metabolism in the development of diabetic complications in relation to metabolic control. 1617 71

The kidney function can be assessed by a number of methods. The urinary excretion of enzymes, in particular N-acetyl-beta-D-glucosaminidase (NAG), is considered a relatively simple, cheap, fast and non-invasive method in the detection and follow-up of renal tubular function under various conditions. The determination of urinary NAG provides a very sensitive and reliable indicator of renal damage, such as injury or dysfunction due to diabetes mellitus, nephrotic syndrome, inflammation, vesicoureteral reflux, urinary tract infection, hypercalciuria, urolithiasis, nephrocalcinosis, perinatal asphyxia, hypoxia, hypertension, heavy metals poisoning, treatment with aminoglycosides, valproate, or other nephrotoxic drugs. This paper gives an overview of the current use of urinary NAG in the detection of renal injury.
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PMID:The diagnostic role of urinary N-acetyl-beta-D-glucosaminidase (NAG) activity in the detection of renal tubular impairment. 1625 16

Cadmium is a well-known nephrotoxic agent in food and tobacco, but the exposure level that is critical for kidney effects in the general population is not defined. Within a population-based women's health survey in southern Sweden (Women's Health in the Lund Area, WHILA), we investigated cadmium exposure in relation to tubular and glomerular function, from 1999 through early 2000 in 820 women (71% participation rate) 53-64 years of age. Multiple linear regression showed cadmium in blood (median, 0.38 microg/L) and urine (0.52 microg/L; density adjusted = 0.67 microg/g creatinine) to be significantly associated with effects on renal tubules (as indicated by increased levels of human complex-forming protein and N-acetyl-beta-D-glucosaminidase in urine), after adjusting for age, body mass index, blood lead, diabetes, hypertension, and regular use of nephrotoxic drugs. The associations remained significant even at the low exposure in women who had never smoked. We also found associations with markers of glomerular effects: glomerular filtration rate and creatinine clearance. Significant effects were seen already at a mean urinary cadmium level of 0.6 microg/L (0.8 microg/g creatinine). Cadmium potentiated diabetes-induced effects on kidney. In conclusion, tubular renal effects occurred at lower cadmium levels than previously demonstrated, and more important, glomerular effects were also observed. Although the effects were small, they may represent early signs of adverse effects, affecting large segments of the population. Subjects with diabetes seem to be at increased risk.
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PMID:Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. 1626 22


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