Background. Adverse maternal environments may predispose the offspring to metabolic syndrome in adulthoods, but the\r\nunderlying mechanism has not been fully understood. Methods. Maternal hyperglycemia was induced by streptozotocin (STZ)\r\ninjection while control (CON) rats received citrate buffer. Litters were adjusted to eight pups per dam and then weaned to standard\r\ndiet. Since 13 weeks old, a subset of offspring from STZ and CON dams were switched to high fat diet (HFD) for another 13\r\nweeks. Glucose and insulin tolerance tests (GTT and ITT) and insulin secretion assay were performed; serum levels of lipids and\r\nleptin were measured. Hepatic fat accumulation and islet area were evaluated through haematoxylin and eosin staining. Results.\r\nSTZ offspring exhibited lower survival rate, lower birth weights, and growth inhibition which persisted throughout the study.\r\nSTZ offspring on HFD showed more severe impairment in GTT and ITT, and more profound hepatic steatosis and more severe\r\nhyperlipidemia compared with CON-HFD rats. Conclusions. Offspring from diabetic dams would be prone to exhibit low birth\r\nweight and postnatal growth inhibition, but could maintain normal glucose tolerance and insulin sensitivity. HFD accelerates\r\ndevelopment of insulin resistance in the offspring of diabetic dams mainly via a compensatory response of islets.
Loading....