Effects Of STZ-induced Hyperglycemia In Male Rats On The Growth, Development And Metabolism In The Offspring

Background: The metabolic syndrome (MetS) is a risk factor thatleads to diabetes and cardiovascular disease. It is characterized by obesity,hypertension and hyperglycemia. In children and adolescents, the prevalenceof metabolic syndrome is in a sharp increase worldwide. Its prevalence is upto6.6%in Guangzhou. Genetic factor plays an important role in thedevelopment of diabetes. Epidemiological study showed, that comparedwith those from healthy parents, the offspring were susceptible to diabeteswith either side of the parents suffering from diabetes. Clinical studiessuggested that there was a close relationship between diabetes with theintrauterine environment. There is, however, a debate on the effect ofpaternal diabetes. Low birth weight, resulted from paternal diabetes, plays akey role in the diabetes development during their adulthood. Studies suggestthat paternal diabetes may play a role through certain susceptibility genes.Therefore, we observed the effect of paternal hyperglycemia on the birthweight and metabolism in the offspring by establishing the malehyperglycemia model. Methods: In STZ group, hyperglycemia was induced by intraperitonealinjection of streptozotocin (STZ)35mg/kg in the healthy adult maleSprague-Dawley rats, while the rats in control group (CON) were receivedcitrate buffer injection. The rats from both groups were allowed to mate withfemale SD rats. The litter size and birth weight of the pups were recorded.The numbers of the pups were adjusted to8per litter. The pups were weanedafter21days, and then the body weights were recorded weekly. Randomblood glucose levels were monitored at week12. Half of rats in both groupsreceived high-fat-diet (HFD) respectively, and the rest received standard diet.Glucose and insulin tolerance test (GTT and ITT) were performed at weeks6in HFD groups. At week18and week22, GTT and ITT were performed onthe rest rats. Insulin secretion test was performed at week22. The animalswere sacrificed, results of the liver/body mass index and serum biochemicalanalysis were compared between the groups.Results: The pups from STZ group showed lower birth weights andslower growth rates resulted possibly from less food intakes in this group.After high-fat diet feeding for6weeks, animals from STZ-H and CON-Hgroup showed a reduced glucose tolerance and insulin tolerance.Interestingly, there was increased insulin sensitivity in STZ offspring at theage of22weeks. Compared with rats from control group, offspring of STZanimals had significantly higher levels of TG.Conclusions: The results showed that paternal hyperglycemia can lead to low birth weight and slower growth rates in the offspring, which mayresult from decreased appetite and less food intakes. The random bloodglucose level as well as the results of GTT and ITT showed no significantdifference between the two groups. However, the insulin sensitivity of theoffspring from STZ group was significantly higher than that of the controlgroup at weeks22.This study suggested that paternal hyperglycemia resulted to lowerbirth weight and growth rates in the offspring, however with significantlyimproved insulin sensitivity. This result suggested paternal hyperglycemiamay effect as a protective mechanism for their offspring. And diabetes had acertain relevance with acquired growth environment.