In the present study, the classic pathophysiological signs of Diabetes mellitus such as hyperglycemia, polyphagia, polydipsia and polyuria, and lower body-weight gain during gestation were observed in the rats eight days after induction of diabetes, corroborating other studies in rodents [34–36].
The hypoglycemia of OD at PND3 may be explained as an exacerbated response of β-pancreatic cells of these pups due to the excessive hyperglycemic stimulus received in the intrauterine environment [37–39], although other factors may be involved. Low birth weight is the main characteristic of the IUGR and occurs frequently when high doses of STZ are used to induce diabetes [26, 27, 38]. Other studies have shown a reduction in body weight in fetuses of STZ induced-diabetic dams [34, 40]. Data from literature demonstrate that intrauterine growth-restricted pups remain small up to adulthood , corroborating the results of the present study. Cross-fostering studies have shown that neonates of diabetic dams nursed by control rats recovered body weight around the weaning . On the other hand, control pups suckled by diabetic dams presented a progressive delay in growth during neonatal life, with significant decrease in body weight from PND 14 . Diabetic rats present decreased synthesis and milk ejection , and the milk from these animals has reduced levels of lactose, fat and protein , which apparently led to undernutrition in the offspring from nontreated diabetic dams. This factor during lactation period probably contributed with the persistent reduction in body weight in OD pups.
The increase in the ages of testicular descent and preputial separation in OD group may suggest that IUGR, besides impairing the normal growth and development of the male offspring, provokes retardation of the initial sexual development of these animals. Others studies corroborate our results showing that early malnutrition and consequent IUGR delay the onset of puberty in rats, associated or not with a body weight reduction [22, 44, 45]. Earlier reports have clearly shown that abnormal intrauterine environment affects the development of several fetal tissues and organs postnatally [46–48]. The present findings indicate impaired growth of male reproductive organs which may be explained, at least in part, due to the low body weight presented by these animals, since these same parameters, when analyzed in relation to body weight, were not significant.
The results of the histological analyses showed that the growth restriction caused by the maternal diabetes during gestation and lactation, did not impair the structural organization of the male offspring gonads, at any point during sexual development. At PND60 the reduction in testicular and epididymal sperm counts seem to be related to the smaller weight of these organs, since they were not significant when analyzed in relation to body weight. On the other hand, in adulthood the sperm reserves in the epididymal cauda were diminished independently of body weight reduction. Animals born from mothers exposed to protein restriction during gestation, another model of IUGR, showed a reduction in sperm reserves in adulthood, corroborating the result of the present study .
As a consequence of the decrease in sperm reserves in the cauda, the sperm transit time was accelerated in this epididymal region. The sperm transit time is a process regulated by androgens, which control the viscosity of epididymal luminal fluid and the contractility of the duct . Other factors such as adrenergic, cholinergic, nonadrenergic noncholinergic innervation  and angiotensins, vasopressins and ocytocins in the blood  may act in the contractility of epididymal duct, interfering in the sperm transit. The accelerated transit of sperm through the epididymis promotes lower exposure of the gametes to the epididymal microenvironment which is crutial to the processes of sperm maturation [53, 54]. Since plasma testosterone levels did not differ between male offspring of control and diabetic dams in the present study, the alteration of sperm transit time through the epididymis appears to have been independent of androgen action.
Recently, a clear relationship between low birth weight and adult renal disease has been stablished, probably related to the reduction of nephron endowment. Data in the literature suggests that individuals with IUGR have 70% greater risk of developing chronic kidney disease in adulthood [55, 56]. Considering that epididymis and kidney structures have a common embrionary origin from Wolffian ducts  these results on renal diseases associated to IUGR may indicate a possible impairment on epididymal development and function at adulthood. Future studies are necessary to investigate the responsible mechanisms for this modification of sperm transit time through the epididymis and the possible consequences on sperm quality.
Nowadays, concern regarding intergenerational studies is well stablished, not only due to genetic factors but also to epigenetic mechanisms . Burdge and co-authors  showed that alterations in the methylation status in specific genes of rat pups (F1) exposed to protein restriction during pregnancy can be transferred to subsequent generations, assuring the importance of epigenetic mechanisms. More investigations are necessary to evaluate the multigenerational effects of in utero and lactational exposure to a hyperglycemic environment.