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https://www.arca.fiocruz.br/handle/icict/26820
INHIBITION OF CELLULAR AUTOPHAGY IN PROXIMAL TUBULAR CELLS OF THE KIDNEY IN STREPTOZOTOCIN-DIABETIC AND UNINEPHRECTOMIZED RATS
Morfometria Ultraestrutural
Túbulos Proximal
Hipertrofia Adaptativa
Uninephrectomy-Diabetes Experimental
Ultrastructural morphometry
Proximal tubules
Adaptative hypertrophy
Uninephrectomy-Experimental diabetes
Author
Affilliation
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
University of Bonn. Department of Pathology. Federal Republic of Germany, Germany
University of Bonn. Department of Pathology. Federal Republic of Germany, Germany
University of Bonn. Department of Pathology. Federal Republic of Germany, Germany
University of Zagreb. Stomatological Faculty. Department of Biology. Yugoslavia
University of Bonn. Department of Pathology. Federal Republic of Germany, Germany
University of Bonn. Department of Pathology. Federal Republic of Germany, Germany
University of Bonn. Department of Pathology. Federal Republic of Germany, Germany
University of Bonn. Department of Pathology. Federal Republic of Germany, Germany
University of Zagreb. Stomatological Faculty. Department of Biology. Yugoslavia
University of Bonn. Department of Pathology. Federal Republic of Germany, Germany
Abstract
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
Keywords in Portuguese
Autofagia CelularMorfometria Ultraestrutural
Túbulos Proximal
Hipertrofia Adaptativa
Uninephrectomy-Diabetes Experimental
Keywords
Cellular autophagyUltrastructural morphometry
Proximal tubules
Adaptative hypertrophy
Uninephrectomy-Experimental diabetes
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