Perinatal stress exposure induced oxidative stress, metabolism disorder, and reduced GLUT-2 in adult offspring of rats.

Abstract

Purpose: Growing evidence has demonstrated that adversity in early life, especially in the prenatal and postnatal period, may change the programming of numerous body systems and cause the incidence of various disorders in later life. Accordingly, this experimental animal study aimed to investigate the effect of stress exposure during perinatal (prenatal and/or postnatal) on the induction of oxidative stress in the pancreas and its effect on glucose metabolism in adult rat offspring.

Methods: In this experimental study based on maternal exposure to variable stress throughout the perinatal period, the pups were divided into eight groups, as follows: control group (C); prepregnancy, pregnancy, lactation stress group (PPPLS); prepregnancy stress group (PPS); pregnancy stress group (PS); lactation stress group (LS); prepregnancy, pregnancy stress group (PPPS); pregnancy, lactation stress group (PLS); and prepregnancy, lactation stress group (PPLS). Following an overnight fast on postnatal day (PND) 64, plasma glucose, insulin, leptin levels, and lipid profiles were evaluated in the offspring groups. GLUT-2 protein levels, lipid peroxidation, antioxidant status, and number of beta-cells in the pancreatic islets of Langerhans as well as the weights of intra-abdominal fat and adrenal glands were assessed. Levels of plasma corticosterone were determined in the different groups of mothers and offspring.

Results: The levels of plasma corticosterone, insulin, and HOMA-B index increased, whereas glucose level and QUICKI index were reduced in the perinatal stress groups compared to C group (p < 0.001 to p < 0.05). Plasma triglyceride, LDL, and cholesterol level rose significantly, but HDL level decreased in the perinatal stress groups compared to C group (p < 0.001 to p < 0.05). Perinatal stress raised MDA concentrations and reduced the activities of antioxidant enzymes in plasma and pancreas compared to C group (p < 0.001 to p < 0.05). GLUT-2 protein levels and number of beta-cells in the stress groups declined compared to C group (p < 0.001 to p < 0.05). Intra-abdominal fat weight decreased in the PPS, PS, and LS groups compared to C group (p < 0.001 to p < 0.01), but adrenal gland weight remained unchanged.

Conclusion: Our results showed that long-term exposure to elevated levels of corticosterone during critical development induces metabolic syndrome in adult male rats.