PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Pancreas Transplantation Delays the Progression of Morphological, Morphometric and Ultrastructural Changes in Testes of Alloxan-Induced Diabetic Rats.

Abstract Aim: The aim of this study was to assess the effects of pancreas transplantation on the progression of testicular lesions in diabetic rats. Methods: Diabetic rats were subjected to pancreas transplantation and sacrificed after 6, 14, 26 and 50 weeks of follow-up, using non-diabetic and untreated diabetic rats as controls. Results: Successful pancreas transplantation corrected all of the metabolic changes observed in diabetic rats, including low levels of testosterone. The testicular mass was decreased, and the relative weight of the testes was high in diabetic rats. The seminiferous tubules of diabetic rats showed progressive atrophy of the germinal epithelium, with cytoplasmic vacuolization, detachment of germ cells to the tubular lumen and the appearance of giant cells. Leydig cells were abnormally distributed, and hyperplasia of Sertoli cells was observed. Sperm were not detectable within the tubular lumen in late follow-up. The diameter, total area, lumen area, and germinal epithelium area of the seminiferous tubules were low, and tubular density was high in diabetic rats. Ultrastructural changes were also observed in these rats, compromising the cytoplasm, organelles and cellular nuclei of the germ, Sertoli, and Leydig cells. The most frequent changes consisted of accumulation of lipid droplets and electron-dense dark material in the cell cytoplasm, cellular degeneration and apoptosis. Similar to non-diabetic rats, pancreas-transplanted rats showed progressive testicular lesions, but they were much less severe and occurred much later than in the untreated diabetic controls. Conclusion: Diabetes causes morphological and ultrastructural changes in rat testes, but the progression of lesions can be significantly delayed by successful pancreas transplantation, which may have a positive impact on male infertility due to diabetes.
PMID
Related Publications
Authors

Mayor MeshTerms
Keywords
Journal Title experimental and clinical endocrinology & diabetes : official journal, german society of endocrinology [and] german diabetes association
Publication Year Start




PMID- 28249332
OWN - NLM
STAT- In-Process
DA  - 20170301
LR  - 20170301
IS  - 1439-3646 (Electronic)
IS  - 0947-7349 (Linking)
VI  - 125
IP  - 2
DP  - 2017 Feb
TI  - Pancreas Transplantation Delays the Progression of Morphological, Morphometric
      and Ultrastructural Changes in Testes of Alloxan-Induced Diabetic Rats.
PG  - 106-115
LID - 10.1055/s-0042-122137 [doi]
AB  - Aim: The aim of this study was to assess the effects of pancreas transplantation 
      on the progression of testicular lesions in diabetic rats. Methods: Diabetic rats
      were subjected to pancreas transplantation and sacrificed after 6, 14, 26 and 50 
      weeks of follow-up, using non-diabetic and untreated diabetic rats as controls.
      Results: Successful pancreas transplantation corrected all of the metabolic
      changes observed in diabetic rats, including low levels of testosterone. The
      testicular mass was decreased, and the relative weight of the testes was high in 
      diabetic rats. The seminiferous tubules of diabetic rats showed progressive
      atrophy of the germinal epithelium, with cytoplasmic vacuolization, detachment of
      germ cells to the tubular lumen and the appearance of giant cells. Leydig cells
      were abnormally distributed, and hyperplasia of Sertoli cells was observed. Sperm
      were not detectable within the tubular lumen in late follow-up. The diameter,
      total area, lumen area, and germinal epithelium area of the seminiferous tubules 
      were low, and tubular density was high in diabetic rats. Ultrastructural changes 
      were also observed in these rats, compromising the cytoplasm, organelles and
      cellular nuclei of the germ, Sertoli, and Leydig cells. The most frequent changes
      consisted of accumulation of lipid droplets and electron-dense dark material in
      the cell cytoplasm, cellular degeneration and apoptosis. Similar to non-diabetic 
      rats, pancreas-transplanted rats showed progressive testicular lesions, but they 
      were much less severe and occurred much later than in the untreated diabetic
      controls. Conclusion: Diabetes causes morphological and ultrastructural changes
      in rat testes, but the progression of lesions can be significantly delayed by
      successful pancreas transplantation, which may have a positive impact on male
      infertility due to diabetes.
CI  - (c) Georg Thieme Verlag KG Stuttgart . New York.
FAU - Tadeu Spadella, Cesar
AU  - Tadeu Spadella C
AD  - Surgery and Orthopedics, Botucatu School of Medicine - UNESP, Botucatu, Brazil.
FAU - Teixeira Trindade, Amelia Arcangela
AU  - Teixeira Trindade AA
AD  - Medicine Course, Federal University of Sao Carlos - UFSCAR, Medicine, Sao Carlos,
      Brazil.
FAU - Natalia Lucchesi, Amanda
AU  - Natalia Lucchesi A
AD  - Faculty of Medicine of Botucatu, UNESP, Graduate Program in General Basis of
      Surgery, Botucatu, Brazil.
FAU - Sperandeo de Macedo, Celia
AU  - Sperandeo de Macedo C
AD  - Faculty of Medicine of Botucatu, UNESP, Pediatrics, Botucatu, Brazil.
LA  - eng
PT  - Journal Article
DEP - 20170301
PL  - Germany
TA  - Exp Clin Endocrinol Diabetes
JT  - Experimental and clinical endocrinology & diabetes : official journal, German
      Society of Endocrinology [and] German Diabetes Association
JID - 9505926
EDAT- 2017/03/02 06:00
MHDA- 2017/03/02 06:00
CRDT- 2017/03/02 06:00
AID - 10.1055/s-0042-122137 [doi]
PST - ppublish
SO  - Exp Clin Endocrinol Diabetes. 2017 Feb;125(2):106-115. doi:
      10.1055/s-0042-122137. Epub 2017 Mar 1.

<?xml version="1.0" encoding="UTF-8"?>
<b:Sources SelectedStyle="" xmlns:b="http://schemas.openxmlformats.org/officeDocument/2006/bibliography"  xmlns="http://schemas.openxmlformats.org/officeDocument/2006/bibliography" >
</b:Sources>