ArticleReproductive biology and endocrinology : RB&E2011
Short- and long-term reproductive effects of prenatal and lactational growth restriction caused by maternal diabetes in male rats.
Article in Reproductive biology and endocrinology : RB&E, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 29 citations in OpenAlex.
- From Maternal Exposure to F1 Development: Unveiling Cyclophosphamide-Induced Reproductive Toxicity.Biomedicines · 2026Article
- Histomorphometric and oxidative evaluation of the offspring's testis from type 2 diabetic female rats treated with metformin and pentoxifylline.International journal of experimental pathology · 2022Review
- Looking at the Future Through the Mother's Womb: Gestational Diabetes and Offspring Fertility.Endocrinology · 2021Review
- Effects of insulin and metformin on fetal kidney development of streptozotocin-induced gestational diabetic albino rats.Anatomy & cell biology · 2019Article
- Maternal diabetes impairs the initiation of meiosis in murine female germ cells.Molecular medicine reports · 2017Article
- Maternal obesity and diabetes may cause DNA methylation alteration in the spermatozoa of offspring in mice.Reproductive biology and endocrinology : RB&E · 2014Article
- Standard operating procedures for maintaining cleanliness in a novel compact facility for breeding SPF mice.Journal of the American Association for Laboratory Animal Science : JAALAS · 2013Article
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7 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundA 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.
methodsMaternal 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.
resultsBody 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.
conclusionsIt 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.
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