We are analyzing https://link.springer.com/article/10.1007/bf02890439.

Title:
Inhibition of cellular autophagy in proximal tubular cells of the kidney in streptozotocin-diabetic and uninephrectomized rats | Virchows Archiv B Cell Pathology
Description:
To examine the significance of anti-catabolism in renal hypertrophy, cellular autophagy was investigated by electron microscopic morphometry in proximal tubular cells (PTCs) of the outer cortex of the rat kidney after the induction of diabetes mellitus by streptozotocin (STZ) and after unilateral nephrectomy. Adult male Sprague-Dawley rats were divided into three groups and killed by retrograde perfusion fixation, 1, 2 and 3 days after the induction of diabetes (group D; n=24), after unilateral nephrectomy (group N; n=24) and after combined treatment (group DN; n=24). Untreated, agematched litter mates served as controls (group C; n=24). By comparison with these controls, the left kidney to initial body weight ratio was increased by 8, 23, and 15% in group D animals, by 8, 23, and 24% in group N animals, and by 10, 21, and 25% in group DN animals at the first, second and third day, respectively. Quantitative evaluation of large test areas showed that the volume and numerical densities of autophagic vacuoles (AVs) in PTCs were significantly lower in these hypertrophed kidneys than in the controls. The average reduction in AV volume density was about 65% in group D animals, about 50% in group N animals and about 75% in group DN animals. These data show that autophagic degradation of cytoplasmic components in PTCs is inhibited in renal hypertrophy independently of the growth stimulus, i.e. uninephrectomy or diabetes. Since insulin per se inhibits cellular autophagy in PTCs, the expected effect of insulin dificiency seems to be counteracted by as yet undefined stimuli that may be related to metabolic work load.
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Keywords {🔍}

google, scholar, cas, pubmed, article, renal, diabetes, kidney, rats, hypertrophy, pfeifer, autophagy, cellular, rat, diabetic, group, degradation, inhibition, mellitus, autophagic, effect, diabetologia, virchows, cells, cell, pathol, animals, growth, insulin, early, physiol, int, privacy, cookies, content, proximal, tubular, jurilj, streptozotocin, unilateral, nephrectomy, functional, arch, exp, liver, biochem, glaumann, osterby, seyerhansen, function,

Topics {✒️}

month download article/chapter diabetic nephropathy rats lysosomen und autophagie isolated autophagic vacuoles-lysosomes proximal tubular cells electron microscopic morphometry full article pdf article virchows archiv kidney tubules privacy choices/manage cookies seyer-hansen streptozotocin-induced diabetes sprague-dawley rats cardiac cellular autophagy initial renal growth related subjects dapagliflozin restores autophagy rat liver induced experimental diabetes mellitus diabetic kidney hyperfunction streptozotocin diabetic rats streptozotocin-diabetic rats renal hypertrophy independently article barbosa sutherland der elevated renal na+ morphological renal manifestations reduced renal mass compensatory renal hypertrophy european economic area thick ascending limb autophagic vacuolar system potentially adverse response leber und niere rytter-nörgaard jo comparative autoradiographic studies 3h-thymidine uptake kidney tissue somatomedin proc vth int electron microscopic cytology conditions privacy policy glomerular ultrafiltration dynamics basement membrane material compensatory kidney growth metabolic work load check access ampk/mtor pathway long-lived proteins instant access short-term stimulation

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         headline:Inhibition of cellular autophagy in proximal tubular cells of the kidney in streptozotocin-diabetic and uninephrectomized rats
         description:To examine the significance of anti-catabolism in renal hypertrophy, cellular autophagy was investigated by electron microscopic morphometry in proximal tubular cells (PTCs) of the outer cortex of the rat kidney after the induction of diabetes mellitus by streptozotocin (STZ) and after unilateral nephrectomy. Adult male Sprague-Dawley rats were divided into three groups and killed by retrograde perfusion fixation, 1, 2 and 3 days after the induction of diabetes (group D; n=24), after unilateral nephrectomy (group N; n=24) and after combined treatment (group DN; n=24). Untreated, agematched litter mates served as controls (group C; n=24). By comparison with these controls, the left kidney to initial body weight ratio was increased by 8, 23, and 15% in group D animals, by 8, 23, and 24% in group N animals, and by 10, 21, and 25% in group DN animals at the first, second and third day, respectively. Quantitative evaluation of large test areas showed that the volume and numerical densities of autophagic vacuoles (AVs) in PTCs were significantly lower in these hypertrophed kidneys than in the controls. The average reduction in AV volume density was about 65% in group D animals, about 50% in group N animals and about 75% in group DN animals. These data show that autophagic degradation of cytoplasmic components in PTCs is inhibited in renal hypertrophy independently of the growth stimulus, i.e. uninephrectomy or diabetes. Since insulin per se inhibits cellular autophagy in PTCs, the expected effect of insulin dificiency seems to be counteracted by as yet undefined stimuli that may be related to metabolic work load.
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      headline:Inhibition of cellular autophagy in proximal tubular cells of the kidney in streptozotocin-diabetic and uninephrectomized rats
      description:To examine the significance of anti-catabolism in renal hypertrophy, cellular autophagy was investigated by electron microscopic morphometry in proximal tubular cells (PTCs) of the outer cortex of the rat kidney after the induction of diabetes mellitus by streptozotocin (STZ) and after unilateral nephrectomy. Adult male Sprague-Dawley rats were divided into three groups and killed by retrograde perfusion fixation, 1, 2 and 3 days after the induction of diabetes (group D; n=24), after unilateral nephrectomy (group N; n=24) and after combined treatment (group DN; n=24). Untreated, agematched litter mates served as controls (group C; n=24). By comparison with these controls, the left kidney to initial body weight ratio was increased by 8, 23, and 15% in group D animals, by 8, 23, and 24% in group N animals, and by 10, 21, and 25% in group DN animals at the first, second and third day, respectively. Quantitative evaluation of large test areas showed that the volume and numerical densities of autophagic vacuoles (AVs) in PTCs were significantly lower in these hypertrophed kidneys than in the controls. The average reduction in AV volume density was about 65% in group D animals, about 50% in group N animals and about 75% in group DN animals. These data show that autophagic degradation of cytoplasmic components in PTCs is inhibited in renal hypertrophy independently of the growth stimulus, i.e. uninephrectomy or diabetes. Since insulin per se inhibits cellular autophagy in PTCs, the expected effect of insulin dificiency seems to be counteracted by as yet undefined stimuli that may be related to metabolic work load.
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      pageEnd:366
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         Ultrastructural morphometry
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         Adaptative hypertrophy
         Uninephrectomy-Experimental diabetes
         Pathology
         Cell Biology
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