Center of Biological and Health Sciences (CCBS), State University of West Paraná (UNIOESTE), Cascavel, Paraná, Brazil.
Reprod Biol Endocrinol. 2011 Dec 6;9:154. doi: 10.1186/1477-7827-9-154.
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.
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.
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.
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.
宫内环境不佳可能对性腺发育产生不利影响，从而增加成年后患生殖障碍和不孕的风险。在这里，我们使用不受控制的母体糖尿病作为模型来引发产前和围产期生长受限，并评估雄性大鼠后代的性发育。
在交配前 7 天，通过单次静脉注射 40mg/kg链脲佐菌素诱导母鼠糖尿病。诱导后血糖水平超过 200mg/dL 的雌性大鼠被选为实验对象。雄性后代在性发育的不同阶段，即青春期前、青春期后和成年期进行分析。
与对照组相比，糖尿病母鼠后代的幼仔在出生后第 3 天的体重和血糖水平较低。母体糖尿病还引起睾丸下降延迟和包皮分离延迟。在糖尿病母鼠的后代中，40、60 和 90 天大的生殖器官重量较低，精子储备和精子通过附睾的转运时间也较短。然而，实验组之间的血浆睾酮水平没有差异。
很难将直接来自糖尿病的影响与宫内发育迟缓的影响分开。尽管在产前和哺乳期暴露于高血糖环境会延迟雄性大鼠青春期的开始，但在所研究的模型中，宫内发育迟缓并未在性发育的任何阶段影响雄性后代的性腺结构组织。然而，附睾尾部精子储备减少和附睾这部分精子转运时间加速可能导致这些动物的精子质量和生育潜力受损。需要进一步研究试图调查母体糖尿病引起的宫内生长受限动物的生育能力和可能的多代影响。
