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)

GAG metabolism was investigated in rats with experimentally induced diabetes. In comparison to control animals, the uptake of 35S-sulfate was diminished in tissues of diabetic animals. Streptozotocin-induced diabetes showed a significant decrease in the content of GAG fractions except that of non-sulfated GAG in liver and kidney which was unchanged as compared to the control group. In rats rendered diabetic by alloxan, non-sulfated GAG increased appreciably in liver and kidney whereas highly sulfated GAG remained unchanged. In the skins of alloxan-diabetic rats both total and sulfated GAG decreased significantly. The activities of liver beta-glucuronidase, beta-N-acetyl glucosaminidase and cathepsin D were significantly increased in rats treated with streptozotocin and alloxan. In streptozotocin-diabetic rats, renal beta-glucuronidase and beta-N-acetyl glucosaminidase activities were reduced while cathepsin D activity was similar to that of controls. The renal beta-N-acetyl glucosaminidase and cathepsin D activities of alloxan-treated rats were not significantly different from normal but their beta-glucuronidase was significantly increased. In the spleen of streptozotocin-diabetic rats all the enzymes were increased except beta-N-acetyl glucosaminidase which remained unaltered. Increased excretion of uronic acid was observed in diabetic groups. These results collectively indicate that both streptozotocin- and alloxan-induced diabetes altered the synthesis and catabolism of GAG.
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PMID:Influence of streptozotocin- and alloxan-induced diabetes on the metabolism of glycosaminoglycans. 624 Jan 83

The activity of collagenase and certain lysosomal hydrolases (cathepsin B1, cathepsin D, beta-glucuronidase and beta-N-acetyl glucosaminidase) was studied in serum and tissues of rats with streptozotocin- or alloxan-induced diabetes. The activity of serum lysosomal enzymes was increased in both groups (p less than 0.05). Both streptozotocin- and alloxan-diabetic animals showed significantly higher dermal collagenase activity than those of controls (p less than 0.01), but the liver and spleen showed similar activities; there was a significant decrease in the renal collagenase activity of streptozotocin-diabetic rats (p less than 0.05). Comparison of the alloxan- or streptozotocin-treated groups with control animals showed an increase in lysosomal enzymes (cathepsin B1, cathepsin D, beta-glucuronidase and beta-N-acetyl glucosaminidase in skin, liver and spleen) (p less than 0.05) but beta-N-acetyl glucosaminidase was unchanged in the spleen of streptozotocin-diabetic rats. There was no difference in renal cathepsin B1 and D in control versus alloxan-diabetic rats, but there was an increase in beta-glucuronidase and beta-N-acetyl glucosaminidase (p less than 0.05). The streptozotocin-diabetic animals showed decreased activities of renal lysosomal enzymes (p less than 0.05), but similar activity of cathepsin D to the control animals.
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PMID:Influence of streptozotocin- and alloxan-induced diabetes in the rat on collagenase and certain lysosomal enzymes in relation to the degradation of connective tissue proteins. 630 89

As compared to controls and epileptics with controlled seizures, serum beta-glucuronidase enzyme is elevated significantly in epileptics with uncontrolled seizures. The enzyme begins to rise just before the seizure, remains elevated during, and for some time after the seizure and then begins to decline, unless another seizure follows the first seizure. The enzyme is not elevated in controlled diabetes patients without any secondary complications. But the enzyme is also elevated in other pathological conditions which involve increased connective tissue catabolism. However, the enzyme is elevated constantly and all the time in these conditions, in contrast with its elevation in uncontrolled epilepsy only close to the seizures.
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PMID:Beta-glucuronidase in sera of patients with epileptic seizure activity, diabetes and some other disease states. 635 7

In a survey the present possibilities are outlined to get knowledge about diseases of inner organs with the help of enzyme determinations in the urine. Here it is remarkable that changes of the enzyme excretion appear not only in renal disease with acute renal failure, pyelonephritis, glomerulonephritis, renal infarction and nephroptosis but are also to be observed in primarily extrarenal diseases such as diabetes mellitus, hyperthyroidism, thesaurismoses, myocardial infarction, hypertension, acute pancreatitis, epidemic hepatitis, liver cirrhosis, obstructive jaundice and rheumatoid arthritis. The causes of the changes of enzyme excretions are various. Since enzymes of different origin and localisation behave themselves variably, the simultaneous determination of a brush border marker (e.g. alanine aminopeptidase), a lysosomal enzyme (e.g. beta-glucuronidase or N-acetyl glucosaminidase) and a low molecular enzyme (e.g. lysozyme) is of use for the recognition of renal alterations. By the control of activities of urinary enzymes it is possible to get without risk informations about pathobiochemical processes in the kidney which are not to be gained by means of other methods.
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PMID:[Urinary enzyme excretion in diseases of the internal organs]. 636 87

Serum and urinary activities of two acid glycohydrolases, beta-n-acetyl-glucosaminidase and beta-glucuronidase, were significantly higher in a group of diabetic patients when compared to a control group. No significant differences were found between patients without vascular complications and those with retinopathy and/or large vessel disease, while the highest enzyme levels were present in diabetics in poor metabolic control. In diabetics with nephropathy, urinary excretion of both enzymes was further increased, so that the serum/urine activity ratio (greater than 1 in normal subjects and in diabetics without nephropathy) was inverted (less than 1). These data seem to show that the high activity of these enzymes, commonly observed in diabetes mellitus, is related to the illness rather than to its vascular complications, being higher in patients in poor metabolic control. Furthermore serum/urine activity ratio may be a useful indicator in the monitoring of diabetic nephropathy.
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PMID:Serum and urinary activities of beta-N-acetylglucosaminidase and beta-glucuronidase in diabetic patients. 663 27

The intracellular activity of beta-glucuronidase (BG) was determined in peripheral blood neutrophils in 59 patients with diabetes mellitus, 35 females and 24 males, aged from 30 to 90 (mean age 60.2). Semiquantitative cytochemical method of Hayashi et al. was employed (1964). The control group consisted of 70 healthy subjects, 29 males and 41 females, aged from 20 to 90 (mean age 58.7). A decreased intracellular activity of beta-glucuronidase in neutrophils as well as an increase pool of beta-glucuronidase were observed in the patients. The authors discuss the significance of this observation in the elucidation of the mechanisms involved in diminished non-specific immunity of patients with diabetes.
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PMID:[Beta-glucuronidase deficiency in the peripheral neutrophils in diabetes mellitus]. 725 30

The role of ornithine decarboxylase (ODC) and polyamines in kidney hypertrophy is controversial. Since part of this controversy could be related to differences in the model system used by the different authors, we studied the changes in renal ODC and polyamines in six different models of kidney hypertrophy in mice, including compensatory renal hypertrophy produced by unilateral nephrectomy, experimental diabetes, potassium depletion and treatment with hormones such as testosterone, thyroxine and fluorocortisone. Only in the case of renal hypertrophy produced by testosterone administration was there a significant increase in ODC activity and putrescine content in the kidneys. However, the concomitant treatment with difluoromethylornithine (DFMO), an irreversible inhibitor of ODC, as a 2% solution in the drinking water completely abolished the increase of renal ODC, but the kidney weights increased and other androgenic effects, such as the induction of renal beta-glucuronidase, were not affected. Moreover, DFMO-treatment did not prevent the kidney enlargement produced in other types of hypertrophy, even in the cases associated with hyperplasia. The present results support the premise that, at least in mice, the increase in ODC activity and polyamine biosynthesis is not required for kidney growth, and also that in most cases renal enlargement is not accompanied by any increase in the polyamine content.
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PMID:An evaluation of the role of polyamines in different models of kidney hypertrophy in mice. 747 58

The activities of three lysosomal hydrolases and creatinine levels were measured in the plasma and urine of 11 adults (mean age, 28.1 years) with insulin-dependent diabetes mellitus and 14 non-diabetic controls (mean age, 27.9 years). All of the patients were free of diabetic complications and non exhibited microalbuminuria. Fractional enzyme excretion (FEE) values between the two groups of subjects were calculated and compared for the following enzymes: beta-hexosaminidase (N-acetyl-glucosaminidase), beta-glucuronidase and alpha-galactosidase. The FEE value was calculated as the ratio of enzyme clearance to creatinine clearance. Relative to the non-diabetic control group, the FEE value for beta-hexosaminidase was approximately 2-fold lower (P = 0.02) in the diabetic subjects (means, 0.424 vs. 0.242, respectively). The FEE values for beta-glucuronidase and alpha-galactosidase were not significantly different (P > 0.4) between the diabetic and control groups. These easily measured biochemical parameters in blood and urine and the resultant FEE value for beta-hexosaminidase may provide a means of assessing subtle deteriorative changes in renal function which occur in the early stage of diabetes before the onset of clinically evident complications.
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PMID:Decreased renal excretion of beta-hexosaminidase in adults with insulin-dependent diabetes mellitus and normal renal function. 822 63

Diabetics are generally considered at higher risk for periodontitis than non-diabetics. Among diabetics, those with poorer metabolic control have often been found to have more periodontitis. This study investigated the relationship between two crevicular fluid enzymes, beta-glucuronidase (beta G) and lactic dehydrogenase (LDH), and metabolic control in 93 adults with type 1 or 2 diabetes. Metabolic control was evaluated by glycosylated hemoglobin (HbA1c) levels. The most visibly inflamed site was sampled for crevicular fluid enzymes and plaque for microbial assessment. Plaque, calculus, and probing depth were also recorded. Beta-glucuronidase was found at significantly higher levels in patients with poorer diabetic control while LDH levels were not related to control. Using multiple regression analysis, good metabolic control was the only predicting variable for beta-glucuronidase when considered with microbes, probing depth, plaque, calculus, age, duration, and type of diabetes. If beta-glucuronidase is a predictor of periodontal disease activity, diabetics with poor metabolic control are at higher risk for periodontitis.
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PMID:Enzyme activity in crevicular fluid in relation to metabolic control of diabetes and other periodontal risk factors. 839 May 72

We previously reported that both local and systemic factors relevant to the pathogenesis of periodontal disease can increase gingival collagenase activity in rats. Since the degradation of extracellular matrix is an essential feature of periodontal disease and this tissue breakdown requires multiple enzyme interactions, the current study was carried out to determine the effects of bacterial endotoxin (LPS) (a local factor) and diabetes (a systemic factor) on a panel of matrix-degrading enzymes (collagenase, gelatinase, elastase, and beta-glucuronidase) in the gingiva of rats. In addition, the effects of therapy with a semisynthetic tetracycline (minocycline) were investigated. Ten male, Sprague-Dawley rats were made diabetic by IV injection of streptozotocin. Four of the ten rats then received minocycline (10 mg/day) by oral gavage on a daily basis for 3 weeks. Nineteen nondiabetic rats served as controls and 9 of them received 10 microliters of E. coli LPS (10 mg/ml) by injection into the labial gingiva every other day during the last week of the study. The other 10 nondiabetic rats were sham injected with saline into the gingiva. At the end of the 3 week experimental period, gingival tissue and skin were dissected from each rat and extracted for enzyme analysis. Our results showed that diabetes markedly increased the four matrix-degrading enzyme activities in both gingiva and skin. In contrast, local LPS injection increased these enzyme activities in the gingiva alone. Systemic therapy with minocycline completely ameliorated these elevated enzyme levels in diabetic rats in both gingiva and skin. Minocycline added in vitro to the enzyme assay systems containing skin extract from diabetic rats also inhibited collagenase and gelatinase activities, but no inhibition was observed for elastase and beta-glucuronidase activities, indicating that the MMPs and other enzymes were inhibited by minocycline, during diabetes, by indirect and indirect mechanisms, respectively.
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PMID:Local and systemic factors in periodontal disease increase matrix-degrading enzyme activities in rat gingiva: effect of micocycline therapy. 882 70


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