Maternal bitter melon supplementation modulates organ inflammation and oxidative damages in fructose fed offspring born of fructose fed dams

Abstract

The environmental cues in early life, such as maternal nutrition, can profoundly alters individuals’ structural and physiological development, which leads to changes in their postnatal phenotypes and thus influences the adult risk for metabolic diseases. Hence, maternal overnutrition and undernutrition are known to disrupt metabolic homeostasis of offspring. Nevertheless such programming impacts could be corrected, at least in part, through nutraceutical supplementation during pregnancy. For instance, maternal green tea epigallocatechin gallate supplementation improved insulin sensitivity in offspring born of high fat fed dams. Similarly, hyperinsulinemia and dyslipidemia in normal diet fed offspring born of high fructose (F) fed dams could be reversed by supplementing bitter melon juice extract to the F dams (FBM). However, when offspring were also fed F, only serum free fatty acid but not insulin level was normalized in those born of FBM dams. In this study, virgin female rats received control (C), F (60%), or BM-supplemented fructose (FBM; 1%) diet before conception until d 21 of lactation. Weaned offspring were fed to the C or F diet for 20 wk, forming C/C, C/F, F/F, FBM/F groups. Compared to the C/F and FBM/F rats, F/F rats had higher adipose PPARγ gene expression but lower gene methylation at the promoter region. Expression of TNFα, IL-6 and leptin followed that of PPARγ responses to maternal F and FBM. Maternal BM dampened F-induced hepatic inflammation, lowered SOCS3 mRNA level and JNK1 phosphorylation. Malondialdehyde level and JNK1 phosphorylation were lowered but activities of antioxidant enzymes were higher in the brain of FBM/F compared with the F/F group. These findings suggest that organ inflammation and oxidative damages may play a role in phenotypic expression but the plasticity of fetal programming provides a window of opportunity in mitigating some of the adverse effects.