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

Biochemical and myocardial functional changes were determined in rabbits made diabetic with alloxan (100 mg/kg, intravenously, two injections 24 h apart). Alloxan-induced diabetes was characterized by a state of hypoinsulinaemia and hyperglycaemia. After 10 weeks of diabetes, significant decreases in heart and left ventricular weights as well as increased serum and heart triglycerides and cholesterol were observed in the diabetic animals (p less than 0.05). In addition, left ventricular pressure, heart rate and rate of left ventricular pressure development were all decreased in the animals. The diabetic state was also associated with a slight elevation in myocardial calcium and a significant decrease in magnesium levels (p less than 0.05). Subcellular fractionation of diabetic hearts indicated the presence of alterations in myofibrillar and sarcoplasmic reticulum marker enzymes (p less than 0.05). Among the lysosomal enzymes, measured, N-acetyl-beta-glucosaminidase activity was significantly increased in the homogenates of diabetic left ventricles (p less than 0.05). These alterations in hearts of diabetic rabbits may be responsible for some aspects of diabetic cardiomyopathy.
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PMID:Biochemical and functional changes in hearts from rabbits with diabetes. 299 85

Cytochemical studies have been performed on peripheral blood lymphocytes of 68 diabetic subjects, with various conditions of metabolic control, and 15 newly diagnosed insulin-dependent diabetic patients. 20 patients of the 1 group had diabetic retinopathy. In diabetic patients periodic acid Schiff positivity, acid phosphatase, and N-acetyl-beta-glucosaminidase activities of lymphocytes are fairly impaired, particularly in insulin-dependent diabetes. Concerning the alpha-naphthyl-acetate-esterase activity, the percentage of positive cells with coarse granules is significantly reduced (p less than 0.001) in diabetic patients as compared to controls, without difference related to age and sex. These abnormalities are more evident in patients with poor glyco-metabolic control. In patients with newly diagnosed insulin-dependent diabetes we have found a further decrease in alpha-naphthyl-acetate-esterase activity, and an increase in acid phosphatase and N-acetyl-beta-glucosaminidase activities. Cyto-enzymatic activities are not significantly different in subjects with diabetic retinopathy. The results of peripheral lymphocyte enzymatic activities in diabetics could be related to a depression of the cell-mediated immunity and could enhance the infections risk of these patients. Furthermore our data show an altered immunological balance in subjects with newly diagnosed type I diabetes.
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PMID:Cytochemistry of circulating lymphocytes in diabetes mellitus with and without retinopathy and in newly diagnosed type I (insulin dependent) diabetes. 310 78

The isoenzyme pattern of N-acetyl-beta-glucosaminidase (NAG) in serum and urine was studied in two groups of patients with diabetes mellitus and in 30 control subjects. Total NAG activity was significantly (P less than 0.001) increased in the serum and urine of the 20 diabetics with vascular complications, but was insignificantly increased in the 20 diabetics without vascular complications. Ion-exchange chromatography demonstrated the presence of two major isoenzymes of NAG, A and B. The proportion of isoenzyme A activity always exceeded that of isoenzyme B. The proportion of isoenzyme B in serum of diabetics was lower than in controls; the reverse was true for urine of diabetics. The NAG isoenzymes pattern may provide additional diagnostic information regarding diabetic status and complications of diabetes.
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PMID:N-acetyl-beta-glucosaminidase isoenzymes in serum and urine of patients with diabetes mellitus. 319 80

The role of insulin as a possible mediator of the beta-adrenergic agonist stimulation of muscle growth was investigated. To exclude possible action of the beta-agonist on the pancreatic release of insulin, diabetes was induced in rats by a streptozotocin injection (100 mg/kg). Insulin levels were almost not detectable in these rats. Feeding either normal diet or diet containing the beta-adrenergic agonist clenbuterol (10 parts/million) did not alter plasma insulin concentrations. The effects of clenbuterol on muscle and weight gain were determined in diabetic rats given daily insulin replacement (D + I) and fed either a normal diet or clenbuterol-treated diet. Clenbuterol, fed for 1 wk, increased the wet weight of the gastrocnemius, soleus, and extensor digitorum longus muscles (15-23%) in both normal and D + I rats. Although clenbuterol increased body weight gain, it did not alter feed consumption and, therefore, feed efficiency (g gain/g food) was improved. Activities of cathepsin B and N-acetyl-beta-glucosaminidase, but not cathepsin D, were elevated in the soleus muscles of clenbuterol-treated rats. The clenbuterol-induced increase in muscle growth in the insulin-replaced diabetic rats indicated that this beta-adrenergic agonist effect was not mediated by an alteration of circulating levels of insulin, secondary to beta-agonist action on pancreatic insulin release.
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PMID:Clenbuterol-induced muscle growth: investigation of possible mediation by insulin. 331 Jun 57

This investigation was performed in two groups of adult patients, 10 with type I and 10 with type II diabetes mellitus, all with arterial hypertension (160 to 200 mm Hg systolic and 95 to 120 mm Hg diastolic). Captopril, 50 mg twice a day, was administered for 12 weeks and was effective as monotherapy in 16 patients. Mean arterial pressure (+/- s.d.) in type I patients changed from 121.4 +/- 9.6 to 100.2 +/- 10.1 after 4 weeks and to 102.0 +/- 3.8 mm Hg after 12 weeks; in type II patients it changed from 132.8 +/- 5.7 to 123.9 +/- 13.5 after 4 weeks and to 109.1 +/- 11.1 mm Hg after 12 weeks. The differences were statistically significant. In only 4 patients was it necessary to add a thiazide after the first month of therapy. No significant change was induced by captopril in urine output, osmolar clearance, free water clearance inulin, and PAH clearances. No significant change was observed in serum and urine Na+, Cl-, Ca++ and Mg++, whereas a statistically significant reduction was found in the renal clearances of K+ and PO4-. No important change in serum aldosterone was found, while plasma renin activity was increased, as expected. No alterations in urine protein, glucosaminoglycans, gamma GT, and N-acetyl-beta-glucosaminidase were observed during follow-up. All patients maintained good metabolic control of their disease. No neutropenia and orthostatic hypotension were seen. Captopril appears to be an effective and safe drug for lowering blood pressure in diabetic patients, without affecting renal function, electrolyte balance and the metabolic control of diabetes.
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PMID:Captopril in the treatment of hypertension in type I and type II diabetic patients. 353 66

Glucagon receptor levels, glucagon-stimulated and other forms of adenylyl cyclase activity, and regulatory component activity of adenylyl cyclase were determined in hepatic plasma membranes of rats administered streptozotocin without and with insulin to produce varying degrees of hyperglycemia. Receptor levels were assayed by direct binding of the specific probe [125I-Tyr10]-iodoglucagon; regulatory component activity was assayed by the capacity to reconstitute stimulatory regulation in deficient membranes from cyc- S49 murine lymphoma cells. In rats given 150 mg streptozotocin, glucagon stimulation of adenylyl cyclase as well as basal, sodium fluoride, 5' guanylylimidodiphosphate [GMP-P(NH)P] and Mn-dependent activities were reduced 50%, glucagon receptor levels but not affinity were reduced 67%, and regulatory component activity was decreased 50%. In addition, alpha 1-adrenergic receptors and 5'-nucleotidase were similarly reduced in diabetes. However, specific ouabain-inhibitable Na+, K+, ATPase activity was not altered by streptozotocin treatment. The streptozotocin-induced changes were noted within 24 h and became maximal by 120 h after its administration. All of these decreases were partially reversed by in vivo insulin treatment. DNA, cytochrome c oxidase, glucose-6-phosphatase, and N-acetyl-beta-glucosaminidase content in hepatic plasma membrane preparations were not substantially different in diabetic as compared with control animals. The data demonstrate that glucagon-mediated regulation of cyclic AMP formation is deranged in insulin deficiency owing to a combined decrease in receptors, derangement of the coupling mechanism intervening between receptor and adenylyl cyclase, and possibly, an altered basal effector system. Some of these changes appear to reflect a "desensitization-like" phenomenon which may or may not be attributable to the hyperglucagonemia of diabetes mellitus. There also appears to be a concurrent generalized decrease in several but not all plasma membrane receptor and enzymatic proteins. This may be the result of a number of processes among which is the accelerated proteolysis of uncontrolled diabetes.
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PMID:Glucagon-stimulable adenylyl cyclase in rat liver. The impact of streptozotocin-induced diabetes mellitus. 632 32

Streptozotocin diabetes strongly reduced the N-acetyl-beta-glucosaminidase activity in the submaxillary glands of mice. A reciprocal change was observed between the enzyme activity and blood sugar in diabetes. Insulin treatment of th diabetic mice returned the reduced activity to the normal level. Isoelectric focusing analysis showed that the submaxillary gland enzyme was composed of two isozymes having isoelectric points (pI) of 4.8 and 8.8. Only the pI 8.8 isozyme was affected by the diabetes.
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PMID:Reduction of N-acetyl-beta-glucosaminidase activity in the submaxillary glands of streptozotocin diabetic mice. 741 14

A commercial method for N-acetyl-beta-glucosaminidase (NAG) is described for use on a discrete analyser. Timed overnight urine was obtained from 20 healthy volunteers and 60 Type I diabetic patients for estimation of NAG (expressed in relation to creatinine) and albumin excretion rate (AER). The upper reference limit for NAG excretion in the control patients was found to be 0.25 U/mmol creatinine but was abnormally raised in 60% of Type I diabetic patients before any increase in AER (greater than 20 micrograms/min), and in 82% of patients with AER greater than 200 micrograms/min. A positive correlation was found between NAG excretion and AER in Type I diabetes (r = 0.61, p < 0.01), but not with glycaemic control as measured by serum fructosamine levels. We conclude that measurement of NAG excretion in diabetes indicates renal tubular dysfunction or damage before any significant change in albumin excretion rate.
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PMID:Urinary N-acetyl-beta-glucosaminidase activity in type I diabetes mellitus. 776 51

Serum ascorbic acid (AA) is reduced in diabetic patients. Aim of this study was 1) to verify whether such a decrease might be due to an altered urinary excretion of AA, and 2) whether this latter was modified in presence of early diabetic nephropathy with microalbuminuria (albumin excretion rate [AER] > 20 micrograms/min) in a group of 21 patients affected by insulin-dependent (type 1) diabetes mellitus (IDDM) as compared with 13 healthy controls matched for sex, age, dietary AA intake, and creatinine clearance per 1.73 m2 (CCl). Mean serum AA (+/- SD) was lower in diabetics (40.3 +/- 14 microM/l) than in controls (85.1 +/- 23.5 microM/l; p = 0.0001) and there was no difference between serum AA of patients with or without microalbuminuria. Urinary excretion of AA to creatinine x 100 (UAA/Cr) was higher in micro- (n = 6; 4.6 +/- 1.7) as compared to normoalbuminurics (n = 15; 1.6 +/- 0.9) or controls (1.5 +/- 1.2; p = 0.0001). For values exceeding renal threshold of tubular AA reabsorption (39 microM) the regression line of serum AA to UAA/Cr was significantly (p = 0.001) steeper in diabetics than in controls, suggesting an impaired tubular reabsorption of filtered AA in IDDM. The ratio of AA clearance to CCl was moreover related to AER (r = 0.48; p = 0.03) and to blood glucose (r = 0.51; p = 0.01), being unrelated to uric acid clearance, glycosuria and to urinary excretion of both alanine aminopeptidase and N-acetyl-beta-glucosaminidase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal excretion of ascorbic acid in insulin dependent diabetes mellitus. 796 Apr 90

The authors investigated a group of 47 type I diabetics in a prospective study extending over 8 years. Every year they evaluated the albuminuria and the N-acetyl-beta-glucosaminidase (NAG) activity in serum and urine and the results were compared with the state of compensation of diabetes and with the clinical finding on the ocular fundus. During the eight-year period newly manifested microalbuminuria developed in 8 of 32 patients (25%) who at the onset had a normal finding. In patients with newly manifested microalbuminuria the authors found a significant rise of the fructosamine serum concentration (p < 0.05) and at the same time a rise of serum NAG activity (p < 0.05). A positive correlation was proved between the serum NAG activity and glycated haemoglobin (r = 0.67, p < 0.01). In 13 patients (28%) in the course of the eight-year period the finding on the ocular fundus deteriorated. In these patients the NAG serum activity was elevated already at the onset of the investigation, while albuminuria rose in the course of the mentioned period. Dynamic changes of the NAG serum activity along with albuminuria can serve as bio-chemical markers of developing microangiopathy the manifestation of which is hastened by deteriorated compensation of diabetes.
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PMID:[Albuminuria and N-acetyl-beta-glucosaminidase activity in a prospective study of type I diabetics]. 837 66


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