Cargando…

Short- and long-term reproductive effects of prenatal and lactational growth restriction caused by maternal diabetes in male rats

BACKGROUND: A suboptimal intrauterine environment may have a detrimental effect on gonadal development and thereby increases the risk for reproductive disorders and infertility in adult life. Here, we used uncontrolled maternal diabetes as a model to provoke pre- and perinatal growth restriction and...

Descripción completa

Detalles Bibliográficos
Autores principales: Amorim, Elaine MP, Damasceno, Débora C, Perobelli, Juliana E, Spadotto, Raquel, Fernandez, Carla DB, Volpato, Gustavo T, Kempinas, Wilma DG
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248370/
https://www.ncbi.nlm.nih.gov/pubmed/22142502
http://dx.doi.org/10.1186/1477-7827-9-154
_version_ 1782220229421563904
author Amorim, Elaine MP
Damasceno, Débora C
Perobelli, Juliana E
Spadotto, Raquel
Fernandez, Carla DB
Volpato, Gustavo T
Kempinas, Wilma DG
author_facet Amorim, Elaine MP
Damasceno, Débora C
Perobelli, Juliana E
Spadotto, Raquel
Fernandez, Carla DB
Volpato, Gustavo T
Kempinas, Wilma DG
author_sort Amorim, Elaine MP
collection PubMed
description BACKGROUND: A suboptimal intrauterine environment may have a detrimental effect on gonadal development and thereby increases the risk for reproductive disorders and infertility in adult life. Here, we used uncontrolled maternal diabetes as a model to provoke pre- and perinatal growth restriction and evaluate the sexual development of rat male offspring. METHODS: Maternal diabetes was induced in the dams through administration of a single i.v. dose of 40 mg/kg streptozotocin, 7 days before mating. Female rats presenting glycemic levels above 200 mg/dL after the induction were selected for the experiment. The male offspring was analyzed at different phases of sexual development, i.e., peripuberty, postpuberty and adulthood. RESULTS: Body weight and blood glucose levels of pups, on the third postnatal day, were lower in the offspring of diabetic dams compared to controls. Maternal diabetes also provoked delayed testicular descent and preputial separation. In the offspring of diabetic dams the weight of reproductive organs at 40, 60 and 90 days-old was lower, as well as sperm reserves and sperm transit time through the epididymis. However the plasma testosterone levels were not different among experimental groups. CONCLUSIONS: It is difficult to isolate the effects directly from diabetes and those from IUGR. Although the exposure to hyperglycemic environment during prenatal life and lactation delayed the onset of puberty in male rats, the IUGR, in the studied model, did not influenced the structural organization of the male gonads of the offspring at any point during sexual development. However the decrease in sperm reserves in epididymal cauda and the acceleration in sperm transit time in this portion of epididymis may lead to an impairment of sperm quality and fertility potential in these animals. Additional studies are needed in attempt to investigate the fertility of animals with intrauterine growth restriction by maternal diabetes and possible multigenerational effects.
format Online
Article
Text
id pubmed-3248370
institution National Center for Biotechnology Information
language English
publishDate 2011
publisher BioMed Central
record_format MEDLINE/PubMed
spelling pubmed-32483702011-12-30 Short- and long-term reproductive effects of prenatal and lactational growth restriction caused by maternal diabetes in male rats Amorim, Elaine MP Damasceno, Débora C Perobelli, Juliana E Spadotto, Raquel Fernandez, Carla DB Volpato, Gustavo T Kempinas, Wilma DG Reprod Biol Endocrinol Research BACKGROUND: A suboptimal intrauterine environment may have a detrimental effect on gonadal development and thereby increases the risk for reproductive disorders and infertility in adult life. Here, we used uncontrolled maternal diabetes as a model to provoke pre- and perinatal growth restriction and evaluate the sexual development of rat male offspring. METHODS: Maternal diabetes was induced in the dams through administration of a single i.v. dose of 40 mg/kg streptozotocin, 7 days before mating. Female rats presenting glycemic levels above 200 mg/dL after the induction were selected for the experiment. The male offspring was analyzed at different phases of sexual development, i.e., peripuberty, postpuberty and adulthood. RESULTS: Body weight and blood glucose levels of pups, on the third postnatal day, were lower in the offspring of diabetic dams compared to controls. Maternal diabetes also provoked delayed testicular descent and preputial separation. In the offspring of diabetic dams the weight of reproductive organs at 40, 60 and 90 days-old was lower, as well as sperm reserves and sperm transit time through the epididymis. However the plasma testosterone levels were not different among experimental groups. CONCLUSIONS: It is difficult to isolate the effects directly from diabetes and those from IUGR. Although the exposure to hyperglycemic environment during prenatal life and lactation delayed the onset of puberty in male rats, the IUGR, in the studied model, did not influenced the structural organization of the male gonads of the offspring at any point during sexual development. However the decrease in sperm reserves in epididymal cauda and the acceleration in sperm transit time in this portion of epididymis may lead to an impairment of sperm quality and fertility potential in these animals. Additional studies are needed in attempt to investigate the fertility of animals with intrauterine growth restriction by maternal diabetes and possible multigenerational effects. BioMed Central 2011-12-06 /pmc/articles/PMC3248370/ /pubmed/22142502 http://dx.doi.org/10.1186/1477-7827-9-154 Text en Copyright ©2011 Amorim et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Amorim, Elaine MP
Damasceno, Débora C
Perobelli, Juliana E
Spadotto, Raquel
Fernandez, Carla DB
Volpato, Gustavo T
Kempinas, Wilma DG
Short- and long-term reproductive effects of prenatal and lactational growth restriction caused by maternal diabetes in male rats
title Short- and long-term reproductive effects of prenatal and lactational growth restriction caused by maternal diabetes in male rats
title_full Short- and long-term reproductive effects of prenatal and lactational growth restriction caused by maternal diabetes in male rats
title_fullStr Short- and long-term reproductive effects of prenatal and lactational growth restriction caused by maternal diabetes in male rats
title_full_unstemmed Short- and long-term reproductive effects of prenatal and lactational growth restriction caused by maternal diabetes in male rats
title_short Short- and long-term reproductive effects of prenatal and lactational growth restriction caused by maternal diabetes in male rats
title_sort short- and long-term reproductive effects of prenatal and lactational growth restriction caused by maternal diabetes in male rats
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248370/
https://www.ncbi.nlm.nih.gov/pubmed/22142502
http://dx.doi.org/10.1186/1477-7827-9-154
work_keys_str_mv AT amorimelainemp shortandlongtermreproductiveeffectsofprenatalandlactationalgrowthrestrictioncausedbymaternaldiabetesinmalerats
AT damascenodeborac shortandlongtermreproductiveeffectsofprenatalandlactationalgrowthrestrictioncausedbymaternaldiabetesinmalerats
AT perobellijulianae shortandlongtermreproductiveeffectsofprenatalandlactationalgrowthrestrictioncausedbymaternaldiabetesinmalerats
AT spadottoraquel shortandlongtermreproductiveeffectsofprenatalandlactationalgrowthrestrictioncausedbymaternaldiabetesinmalerats
AT fernandezcarladb shortandlongtermreproductiveeffectsofprenatalandlactationalgrowthrestrictioncausedbymaternaldiabetesinmalerats
AT volpatogustavot shortandlongtermreproductiveeffectsofprenatalandlactationalgrowthrestrictioncausedbymaternaldiabetesinmalerats
AT kempinaswilmadg shortandlongtermreproductiveeffectsofprenatalandlactationalgrowthrestrictioncausedbymaternaldiabetesinmalerats