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The aim of the study was the evaluation of changes in the adrenal cortex lysosomal enzymes activity during experimental alloxan-induced diabetes mellitus in rabbits. We checked the activity of acid phosphatase, β-D-galactosidase, N-acetyl-β-D-glucosaminidase (NAGL) and lipase. The study was performed on 124 rabbits divided into five groups: one control and four experimental. Diabetes mellitus was induced by a single injection of 10% alloxan solution into the auricular vein in a dose of 10 mg per kg body weight. Animals from experimental groups were killed in the 21st, 42nd, 90th and 180th days of the study. Adrenal glands were removed. Enzymes activity was assayed by spectrophotometric methods. Changes in free and bound fractions of examined lysosomal enzymes activity were noticed already in the 21st day of diabetes. The most escalated changes were observed in the 42nd day of the study. Performed statistical variance analysis demonstrated statistically highly significant differences for activity of both fractions of NAGL and lipase, as well as for free fraction activity of acid phosphatase and β-D-galactosidase. The obtained data confirmed the influence of diabetes mellitus on changes in the activity of examined lysosomal enzymes in the adrenal cortex.
Chronic isoproterenol administration produces a rapid, highly reproducible rodent model of cardiac hypertrophy. Yet, despite widespread use of this model, the effects of isoproterenol on in vivo cardiac function and substrate metabolism are unknown. Isoproterenol (5 mg.kg-1.day-1) was infused for 7 days in male Wistar rats (n = 22). In vivo magnetic resonance imaging (MRI) showed that left ventricular mass increased by 37% and end-diastolic and systolic volumes increased by 33% and 73%, respectively, following isoproterenol infusion. Cardiac function at the base of the left ventricle was normal, but apical ejection fraction decreased from 90% to 31% and apical free wall thickening decreased by 94%, accompanied by increased fibrosis and inflammation. Myocardial palmitate oxidation rates were 25% lower, and citrate synthase and medium chain acyl-coenzyme A dehydrogenase activities were reduced by 25% and 29%, respectively, following isoproterenol infusion. Fatty acid transporter protein levels were 11-52% lower and triglyceride concentrations were 55% lower in isoproterenol-infused rat hearts. Basal glycolysis and glycogen concentration were not changed, yet insulin stimulated glycolysis was decreased by 32%, accompanied by 33% lower insulin stimulated glucose transporter, GLUT4, protein levels in rat hearts following isoproterenol infusion, compared with controls. In conclusion, isoproterenol infusion impaired in vivo cardiac function, induced hypertrophy, and decreased both fatty acid and glucose metabolism, changes similar in direction and magnitude to those found in the rat heart following moderate severity myocardial infarction.
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