Abstract
Background. Adverse maternal environments may predispose the offspring to metabolic syndrome in adulthoods, but the underlying mechanism has not been fully understood. Methods. Maternal hyperglycemia was induced by streptozotocin (STZ) injection while control (CON) rats received citrate buffer. Litters were adjusted to eight pups per dam and then weaned to standard diet. Since 13 weeks old, a subset of offspring from STZ and CON dams were switched to high fat diet (HFD) for another 13 weeks. Glucose and insulin tolerance tests (GTT and ITT) and insulin secretion assay were performed; serum levels of lipids and leptin were measured. Hepatic fat accumulation and islet area were evaluated through haematoxylin and eosin staining. Results. STZ offspring exhibited lower survival rate, lower birth weights, and growth inhibition which persisted throughout the study. STZ offspring on HFD showed more severe impairment in GTT and ITT, and more profound hepatic steatosis and more severe hyperlipidemia compared with CON-HFD rats. Conclusions. Offspring from diabetic dams would be prone to exhibit low birth weight and postnatal growth inhibition, but could maintain normal glucose tolerance and insulin sensitivity. HFD accelerates development of insulin resistance in the offspring of diabetic dams mainly via a compensatory response of islets.
Highlights
Metabolic syndrome (MetS) is a clustering of metabolic disorders including hyperglycemia, hypertension, dyslipidemia, overweight, and central obesity, with insulin resistance as the central feature of this syndrome [1]
From 13 weeks of age, half of the offsprings in both groups were switched to high fat diet (HFD, 45% of energy from fat, SLAC laboratory animal, China), and the rest were maintained on standard chow diet, and thereby four separate adult offspring groups were studied: CON offspring fed standard chow diet (CON-S), CON offspring fed HFD (CON-H), STZ offspring fed standard chow diet (STZ-S), and STZ offspring fed HFD (STZ-H)
Among the 15 pregnant rats injected with STZ, only 10 rats (66.7%) met our criteria with blood glucose levels all above 20 mM throughout gestational and lactation periods, and glucose levels were 23.3 ± 0.4 mM, 22.8 ± 0.2 mM, 23.1 ± 2.3 mM, and 20.9 ± 2.4 mM on G5, G12, G19, and L10, respectively
Summary
Metabolic syndrome (MetS) is a clustering of metabolic disorders including hyperglycemia, hypertension, dyslipidemia, overweight, and central obesity, with insulin resistance as the central feature of this syndrome [1]. Intrauterine exposure to a hyperglycemic environment predisposes the offspring to develop glucose intolerance and obesity in early life [5,6,7,8,9]. These epidemiological and clinical studies have strongly certified that maternal pregnancy with hyperglycemia was a major risk factor for the development of MetS in their offspring [10, 11]. HFD accelerates development of insulin resistance in the offspring of diabetic dams mainly via a compensatory response of islets
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