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)

N-acetyl-beta-D-glucosaminidase (NAG), a lysosomal enzyme, has been shown to be increased in the urine of patients with various glomerulonephritides, tubulointerestitial diseases, renal allograft rejection, toxic renal injury, and diabetes mellitus. Although it has been suggested that urinary NAG may reflect blood glucose control, no studies have correlated this with other measures of metabolic control. Thirty-four children from a diabetic summer camp were found to have urinary NAG to creatinine ratios significantly above those of normal controls of similar age (5.22 +/- 1.19 versus 1.51 +/- 0.17 U). Urinary NAG was found to positively correlate with an arbitrary control index (r = 0.82; P less than 0.05) and in seven patients with hemoglobin A1c (r = 0.70; P less than 0.001). In a closely followed group of 40 clinic patients, urinary NAG to creatinine ratio was again found to be significantly increased over normal controls (7.55 +/- 0.70 versus 1.51 +/- 0.17 U; P less than 0.05). Again, urinary NAG was positively correlated with HbA1c (r = 0.62; P less than 0.001) and urinary albumin to creatinine ratio (r = 0.47; P less than 0.01). In neither group was there a correlation with UNAG:UCr and duration of disease. Thus, these data suggest that urinary NAG to creatinine ratio appears to be a reflection of blood sugar control.
Diabetes Care
PMID:Urinary excretion of N-acetyl-beta-D-glucosaminidase in children with type I diabetes mellitus. 634 77

The catalytic activities of N-acetyl-beta-D-glucosaminidase, beta-galactosidase and alpha-glucosidase in kidney and urine of diabetic rats were investigated in relation to the duration of diabetes, to the degree of constant hyperglycaemia and to the therapeutic control in the early stage of disease. The results suggest that the degree of constant hyperglycaemia and the duration of untreated diabetes are significant determining factors for the course of morphological changes. These changes are manifested as a decrease of the glycosidases in kidney (0.5 to 0.6 time the age-matched controls) and as moderate to severe enzymurias. Daily variation of blood glucose with inadequate insulin Lente therapy caused decreased N-acetyl-beta-D-glucosaminidase and beta-galactosidase activities in kidney as well as enzymuria. Since such changes can be correlated with histologically visible changes in the kidney, the measurement of these enzymes in urine is a simple way of monitoring the development of kidney damage in poorly controlled diabetes. When constant normoglycaemia was maintained for three weeks with insulin Ultralente in diabetic rats with a confirmed decrease of kidney glycosidases, the persisting morphological alteration of the organ was reflected by a urinary output of N-acetyl-beta-D-glucosaminidase.
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PMID:Effect of the degree of hyperglycaemia on the catalytic activities of glycosidases in kidney and urine of diabetic rats. 636 9

Urinary N-acetyl-beta-D-glucosaminidase (NAG) has been shown to be a sensitive indicator of blood sugar control. Twelve insulin-dependent diabetics whose blood glucoses were being controlled with the artificial pancreas had concurrent urinary NAG activity measured. Blood glucose dropped markedly from 198 +/- 22 mg/dl (x +/- SEM) to 121 +/- 7 mg/dl during the 25 h on the artificial pancreas. For the entire group UNAG: UCr dropped from 14.9 +/- 4.4 to 7.25 +/- 1.68 units. In order to determine if larger decreases in blood glucoses over the course of the study resulted in larger decreases in UNAG: UCr, an arbitrary division at 180 mg/dl was made. Six patients with blood glucoses at or above this level at the start of the study showed a drop in both blood glucoses and UNAG: UCr (261 +/- 24 to 134 +/- 12 mg/dl and 21.1 +/- 6.1 to 7.29 +/- 1.53 U, respectively). Even though the other six patients had blood glucoses below the renal threshold, both blood glucoses and UNAG: UCr declined (136 +/- 4 to 110 +/- 4 mg/dl; 8.89 +/- 2.4 to 6.2 +/- 1.64 U, respectively). Thus not only may urinary NAG activity reflect long-term control and renal complications of diabetes, but this enzyme is also responsive to acute changes in blood glucose.
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PMID:Response of urinary N-acetyl-beta-D-glucosaminidase to rapid decreases in blood glucose. 646 9

Excretion of urinary N-acetyl-beta-D-glucosaminidase has been found to be elevated in diabetic humans and rats. This urinary glycosidase may reflect blood sugar control over time, since it has been significantly and positively correlated with hemoglobin A1 in children with insulin-dependent diabetes. Other studies have suggested that urinary NAG may predict diabetic nephropathy. In order to more carefully define the relationship between urinary NAG excretion and blood and urine sugars, hemoglobin A1, and microalbuminuria, 48 rats were made diabetic by the use of streptozotocin. All rats were uninephrectomized at 3 weeks. Of these, 23 were treated with daily insulin injections, 25 were untreated, and both groups were compared to 13 control, nondiabetic rats. Urine volume, glucose, albumin, and blood sugar were all significantly (P less than 0.05) elevated in the untreated rats compared to the treated and control groups. Urinary NAG:UCr was significantly (P less than 0.01) elevated in the untreated group with lower but still elevated levels (P less than 0.05) in the treated rats. To further define the time course of the increase in UNAG:UCr 12 rats were followed serially at 12-hr intervals for 92 hr after streptozotocin. Urinary NAG increased significantly (P less than 0.05) at 12 hr after streptozotocin injection and reached a plateau at 36 hr while hemoglobin A1 did not rise until 2 weeks after onset of hyperglycemia. Urinary NAG increases more rapidly than hemoglobin A1 after onset of hyperglycemia and glycosuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary N-acetyl-beta-D-glucosaminidase in streptozotocin-induced diabetic rats. 647 35

A prospective study was undertaken of 15 patients with impaired renal function undergoing x-ray procedures entailing the use of contrast material to see whether any deterioration in renal function resulted. Patients with diabetes or myelomatosis were excluded. Detailed observations were made during three days before and after the x-ray procedure to detect any change in factors such as fluid state, drug treatment, infection, or diet which might have affected renal function. No significant changes occurred in endogenous creatinine and 51Cr-EDTA clearances, or in plasma creatinine and urea concentrations after the x-ray procedures. Furthermore, there was no change in urinary activity of N-acetyl-beta-D-glucosaminidase, which is a highly sensitive indicator of renal parenchymal damage. Provided that fluid depletion and multiple x-ray procedures with radiocontrast material in rapid sequence are avoided, these procedures do not appear to affect renal function adversely, even when renal disease is advanced.
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PMID:Effect of radiocontrast media on kidneys of patients with renal disease. 678 30

We conducted an open clinical trial to determine whether administration of iloprost, a stable prostacyclin analog, has any effect on urinary albumin excretion and other parameters associated with non-insulin-dependent diabetes mellitus (NIDDM) patients. Twenty-three NIDDM patients with nephropathy were divided into groups A and B which were matched in terms of sex, age, duration of diabetes and blood glucose control. After 2 weeks of observation, 11 patients in group A received an intravenous infusion of iloprost (10 micrograms at a rate of 0.075 microgram/kg per h) once daily for 2 weeks, while 12 untreated diabetic patients in group B served as controls. In group A, iloprost significantly reduced the urinary albumin excretion rate, the urinary albumin-creatinine ratio and N-acetyl-beta-D-glucosaminidase without decreasing creatinine clearance during the treatment period (P < 0.05, respectively). However, none of these parameters changed significantly in group B. Urinary beta 2-microglobulin, blood pressure, heart rate, serum electrolytes, BUN and serum creatinine were not significantly altered by iloprost during the treatment period. Side effects associated with iloprost were mild and could be ameliorated by slowing the infusion rate. We conclude that iloprost appears to be safe and has an apparent effect on the urinary albumin excretion rate and N-acetyl-beta-D-glucosaminidase.
Diabetes Res Clin Pract
PMID:Iloprost decreases urinary albumin excretion rate in patients with diabetic nephropathy. 750 37

Diabetic nephropathy is usually characterized by glomerular dysfunction; the view that tubular damage occurs as a consequence, however, has been disputed. To verify this hypothesis we compared glomerular with proximal and distal tubular parameters in 62 patients with diabetes mellitus type I. The duration of disease ranged between 0 and 39 years and the glomerular, proximal tubular, and distal tubular parameters were investigated in 24-h urine samples. Excretion of albumin as a marker of the glomerulum, alpha 1-microglobulin and N-acetyl-beta-D-glucosaminidase as parameters of proximal tubule, and Tamm-Horsfall protein as parameter of distal tubule were determined by sensitive enzyme-linked immunosorbent assays. Patients were divided into five groups (D1-D5) according to the duration of diabetes as follows: D1, less than 1 year; D2, 1-4 years; D3, 5-9 years; D4, 10-14 years; D5, longer than 14 years. Healthy individuals (n = 61) aged 3-42 years served as controls. Significantly increased excretion of proximal tubular parameters were found in early course while albumin excretion was still in the normal range. In addition, proximal tubular alpha 1-microglobulin showed an increase during the course of diabetes duration, probably indicating an early proximal tubular impairment. Distal tubular Tamm-Horsfall protein showed increasing excretion in D1-D4, which may reflect disturbance of the thick ascending loop of Henle. Our results therefore stress the importance of tubular parameters such as alpha 1-microglobulin during early diabetes mellitus type I since they may serve as early markers of renal dysfunction and may precede albumin excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal proximal and distal tubular function is attenuated in diabetes mellitus type 1 as determined by the renal excretion of alpha 1-microglobulin and Tamm-Horsfall protein. 751 Jan 55

To assess whether urinary N-acetyl-beta-D-glucosaminidase (NAG) and beta 2-microglobulin (beta 2-MG) levels could be used as predictors of diabetic nephropathy or not, 59 non-insulin-dependent diabetes mellitus (NIDDM) patients were included in our study (31 females, 29 males; mean age 54 +/- 10.1). The control group consisted of 20 healthy non-diabetic subjects (12 males and 8 females; mean age 47 +/- 13.9). The patients in the study group were classified according to the duration of diabetes. In all cases, urinary beta 2-MG levels were measured by specific enzyme immunoassays and urinary NAG enzyme activities were determined by colorimetric methods. The mean urinary NAG level in study group was higher than that of the control group (p < 0.01). It was observed that NAG activity begins to rise in the third year of NIDDM, makes a plateau between 3-10 years, and rapidly increases after the 10th year. No significant difference in NAG activity was found between chemical NIDDM and control groups. No significant difference in beta 2-MG levels was found between study and control groups. The mean NAG activity in patients with early glomerular hyperfiltration was significantly higher than those without early hyperfiltration and control group (p < 0.05), whereas the mean beta 2-MG level was not. As a result, urinary NAG enzyme activity significantly increases, while urinary beta 2-MG level remains unchanged in patients with NIDDM. It was concluded that measurement of urinary NAG enzyme activity may be a good indicator in early diagnosis of diabetic nephropathy.
Diabetes Res 1994
PMID:Urinary beta 2-microglobulin levels and urinary N-acetyl-beta-D-glucosaminidase enzyme activities in early diagnosis of non-insulin-dependent diabetes mellitus nephropathy. 762 16

We investigated the relation between activities of islet glycogenolytic alpha-glucosidehydrolases and insulin secretion induced by glucose and 3-isobutyl-1-methylxanthine (IBMX) by means of suppressing 1) insulin release (Ca2+ deficiency) and 2) islet alpha-glucosidehydrolase activity (selective inhibition by the deoxynojirimycin derivative miglitol). Additionally, the in vivo insulin response to both secretagogues was examined. We observed that, similar to glucose-induced insulin release, islet glycogenolytic hydrolases (acid amyloglucosidase, acid alpha-glucosidase) were highly Ca2+ dependent. Acid phosphatase, N-acetyl-beta-D-glucosaminidase, or neutral alpha-glucosidase (endoplasmic reticulum) was not influenced by Ca2+ deficiency. In Ca2+ deficiency IBMX-induced insulin release was unaffected and was accompanied by reduced activities of islet alpha-glucosidehydrolases. Miglitol strongly inhibited glucose-induced insulin release concomitant with a marked suppression of islet alpha-glucosidehydrolase activities. Direct addition of miglitol to islet homogenates suppressed acid amyloglucosidase [half-maximal effective concentration (EC50) approximately 10(-6) M] and acid alpha-glucosidase. Acid phosphatase and N-acetyl-beta-D-glucosaminidase were unaffected. The miglitol-induced inhibition of glucose-stimulated insulin release was dose dependent (EC50 approximately 10(-6) M) and displayed a remarkable parallelism with the inhibition curve for acid amyloglucosidase. The in vivo insulin secretory response to glucose was markedly reduced in dystrophic mice (low amyloglucosidase), whereas the response to IBMX was unaffected. In summary, islet glycogenolytic hydrolases are Ca2+ dependent, and acid amyloglucosidase is directly involved in the multifactorial process of glucose-induced insulin release. In contrast the mechanisms of IBMX-stimulated insulin secretion operate independently of these enzymes. The effects of miglitol, a drug currently used in diabetes therapy, deserves further investigation.
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PMID:Ca2+ deficiency, selective alpha-glucosidehydrolase inhibition, and insulin secretion. 768 25

Urine albumin, alpha 1- and beta 2-microglobulins, retinol-binding protein (RBP) and N-acetyl-beta-D-glucosaminidase (NAG) were measured in early morning urine samples from 99 non-insulin-dependent diabetic (NIDDM) patients receiving ambulatory care at a primary health care polyclinic. Elevated NAG levels were found in 90% of diabetics regardless of the duration of their disease. Almost half (43.4%) of the subjects had microalbuminuria. Over a third of the subjects without albuminuria had elevated alpha 1-microglobulin levels in their urine. The proportion of subjects with elevated alpha 1 levels increased significantly with the presence of albumin, poor glycaemic control and increased duration of disease. These findings suggest that proximal tubular as well glomerular dysfunction coexist in the NIDDM patients studied.
Diabetes Res Clin Pract 1993 Jun
PMID:Proteinuria and enzymuria in non-insulin-dependent diabetics. 769 91


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