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n acetyl beta d glucosaminidase/obesitat
L'enllaç es desa al porta-retalls
Pàgina 1 des de 26 resultats
Increased serum N-acetyl-beta-D-glucosaminidase and alpha-D-mannosidase activities in obese subjects.
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We have studied N-acetyl-beta-D-glucosaminidase and alpha-D-mannosidase activities in human sera from 35 control subjects, 47 normo- and hyperinsulinemic obese persons, and 12 diabetic patients after a fasting period of 12 h and at 30, 60, 90, and 120 min after an oral glucose overload. The results
Association between nonalbumin proteinuria and renal tubular damage of N-acetyl-β-d-glucosaminidase and its clinical relevance in patients with type 2 diabetes without albuminuria.
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OBJECTIVE
Although albuminuria and urinary N-acetyl-β-d-glucosaminidase (uNAG) are known as progression markers of diabetic kidney disease, there is limited information regarding the association between urinary nonalbumin proteinuria (NAP) and uNAG and the clinical relevance thereof in patients
Progression of renal damage in the obese Zucker rat in response to deoxycorticosterone acetate-salt-induced hypertension.
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This study assessed the progression of renal damage in obese Zucker rats in response to deoxycorticosterone acetate (DOCA)-salt-induced hypertension. Renal damage was evaluated by light microscopy and urine analysis at weekly intervals during the developmental phase of DOCA-salt hypertension and
Effects of soy protein isolate feeding on severe kidney damage in DOCA salt-treated obese Zucker rats.
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This study assessed the effects of soy protein isolate (SPI) on severe kidney damage in deoxycorticosterone acetate (DOCA) salt-treated obese Zucker rats. These rats underwent heminephrectomy and were fed either casein or SPI diet for 12 weeks. From weeks 8 to 10 of the experiment, kidney damage was
Implant-induced inflammatory angiogenesis is up-regulated in obese mice
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The damaging effects of obesity extend to multiple pre-existing tissue/organs. However, the influence of this condition on key components (inflammation and angiogenesis) of fibrovascular connective proliferating tissue, essential in repair processes, has been neglected. Our objective in this study
Early markers of obesity-related renal injury in childhood.
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Childhood obesity has become a global epidemic. Recent epidemiological data suggest that obesity is associated with increased risk of renal injury in children. The onset of obesity-associated renal disease is insidious and asymptomatic, so early markers will be extremely useful in its prevention and
Determination of early urinary renal injury markers in obese children.
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BACKGROUND
Obesity is an important health issue, the prevalence of which is increasing in childhood. The aim of this study was to examine urinary renal injury markers in order to determine the renal effect of obesity and its comorbidities in a pediatric population.
METHODS
Eighty-four obese children
Differential changes in islet lysosomal enzyme activities in aging obese hyperglycemic mice.
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The pattern of pancreatic islet lysosomal enzyme activities was investigated in adult obese mice (aged 5-7 months), old obese mice (aged 9-17 months) and aged-matched old "obese" mice suffering from excessive weight loss. A series of lean NMRI mice of comparable age was included as controls. It was
Urinary PC-1 and N-acetyl-beta-D-glucosaminidase activity in patients with type 2 diabetes treated with metformin, gliclazide or glibenclamide.
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BACKGROUND
Insulin resistance is a key feature of type 2 diabetes mellitus. Plasma cell differentiation antigen (PC-1) is an inhibitor of insulin receptor tyrosine kinase, and has been implicated in the pathogenesis of insulin resistance.
METHODS
Urinary excretion of PC-1 was determined in 45 newly
Lysosomal enzyme activities in pancreatic islets from normal and obese hyperglycemic mice.
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Lysosomal enzyme activities in pancreatic islets of obese hyperglycemic ob/ob mice aged 3 to 6 months were investigated and compared with those of normal lean NMRI mice of the same age. It was observed that the glycogenolytic glucose-producing hydrolase acid amyloglucosidase displayed a fivefold
Influence of remote cancer and obesity on, and distribution of mucosal enzymes in, the upper small intestine.
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A series of mucosal enzymes were estimated by analysis of homogenized biopsy specimens from the lower duodenal flexure, obtained from 10 large-bowel carcinoma patients, 15 patients with morbid obesity, and 15 controls. In 11 subjects the distribution along the upper small intestine was determined.
The prostacyclin analog beraprost sodium ameliorates characteristics of metabolic syndrome in obese Zucker (fatty) rats.
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OBJECTIVE
The prostacyclin analog, beraprost sodium (BPS), was examined for its potential to improve the symptoms of obesity-type diabetes (i.e., hyperglycemia, hyperinsulinemia, dyslipidemia, histopathologic changes, and diabetic complications).
METHODS
Obese Zucker rats, an experimental model of
N-acetyl-beta-D-glucosaminidase in lymphocytes of patients with diabetes mellitus.
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In 55 patients with diabetes mellitus the significant quantitative increase in numbers of N-acetyl-beta-D-glucosaminidase-positive lymphocytes in the peripheral blood has been examined by cytochemical methods. The enzyme-positive lymphocytes of these patients were characterized by prevalence of
Angiotensin II Type 2-Receptor Agonist C21 Reduces Proteinuria and Oxidative Stress in Kidney of High-Salt-Fed Obese Zucker Rats.
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Oxidative and nitrosative stress have been implicated in high-sodium diet (HSD)-related hypertensive renal injury. In this study, we investigated angiotensin II type 2-receptor-mediated renoprotection in obese Zucker rats fed HSD. Obese Zucker rats were fed normal sodium diet or HSD 4%, for 14 days,
Multiple-dose pharmacokinetics and pharmacodynamics of sergliflozin etabonate, a novel inhibitor of glucose reabsorption, in healthy overweight and obese subjects: a randomized double-blind study.
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Sergliflozin, the active entity of sergliflozin etabonate, is a selective inhibitor of the sodium-dependent glucose cotransporter-2 in the renal tubule. The pharmacokinetics and pharmacodynamics of sergliflozin were examined during administration of sergliflozin etabonate (500 or 1000 mg) or placebo
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