Offspring from mothers fed a ‘junk food’ diet in pregnancy and lactation exhibit exacerbated adiposity that is more pronounced in females

Abstract

We have shown previously that a maternal junk food diet during pregnancy and lactation plays a role in predisposing offspring to obesity. Here we show that rat offspring born to mothers fed the same junk food diet rich in fat, sugar and salt develop exacerbated adiposity accompanied by raised circulating glucose, insulin, triglyceride and/or cholesterol by the end of adolescence (10 weeks postpartum) compared with offspring also given free access to junk food from weaning but whose mothers were exclusively fed a balanced chow diet in pregnancy and lactation. Results also showed that offspring from mothers fed the junk food diet in pregnancy and lactation, and which were then switched to a balanced chow diet from weaning, exhibited increased perirenal fat pad mass relative to body weight and adipocyte hypertrophy compared with offspring which were never exposed to the junk food diet. This study shows that the increased adiposity was more enhanced in female than male offspring and gene expression analyses showed raised insulin-like growth factor-1 (IGF-1), insulin receptor substrate (IRS)-1, vascular endothelial growth factor (VEGF)-A, peroxisome proliferator-activated receptor-γ (PPARγ), leptin, adiponectin, adipsin, lipoprotein lipase (LPL), Glut 1, Glut 3, but not Glut 4 mRNA expression in females fed the junk food diet throughout the study compared with females never given access to junk food. Changes in gene expression were not as marked in male offspring with only IRS-1, VEGF-A, Glut 4 and LPL being up-regulated in those fed the junk food diet throughout the study compared with males never given access to junk food. This study therefore shows that a maternal junk food diet promotes adiposity in offspring and the earlier onset of hyperglycemia, hyperinsulinemia and/or hyperlipidemia. Male and female offspring also display a different metabolic, cellular and molecular response to junk-food-diet-induced adiposity.

Established diet-induced obesity in female rats leads to offspring hyperphagia, adiposity and insulin resistance

“…Further support for generation of obesity in the offspring of obese dams comes from Bayol et al, who showed that offspring of rats that were fed a 'junk food' diet (including highly palatable foods such as chocolate, crisps and doughnuts) in pregnancy and lactation developed increased fat mass after weaning on to a normal diet [35,36]. In contrast to the present study, this was more predominant in females than males [35].…”

“…Using an identical diet to that of the present study, we have also recently shown a similar increase in fat mass in the offspring of obese mice, proving commonality of this model in different rodent species [34]. Further support for generation of obesity in the offspring of obese dams comes from Bayol et al, who showed that offspring of rats that were fed a 'junk food' diet (including highly palatable foods such as chocolate, crisps and doughnuts) in pregnancy and lactation developed increased fat mass after weaning on to a normal diet [35,36]. In contrast to the present study, this was more predominant in females than males [35].…”

“…Since we have also observed hyperphagia in the offspring of obese mice fed the same diet [34], persistent alteration in regulation of appetite-controlling pathways may play a causative role in the development of increased adiposity in both species. Food intake has not been rigorously assessed by others addressing the same hypothesis [28], although Bayol et al [35,41] have implicated altered food preference (for 'junk food' over standard chow) in development of obesity in offspring of dams fed the 'junk food' diet throughout pregnancy and lactation, but not when exposed to the diet during pregnancy only. Similarly no difference was shown in food intake in the offspring of obese dams exposed to this obesogenic diet during gestation alone [28].…”

Parental influence on children's early eating environments and obesity risk: implications for prevention

“…Rats with prenatal-only exposure were fatter than those without any exposure, but rats that were exposed to junk food throughout the study had the riskiest outcomes, including the highest levels of adiposity and hyperinsulinemia. 46 In a similar 2 Â 2 experimental design, offspring of dams fed high-fat chow during pregnancy had higher adult body weights and blood pressure than offspring who experienced a standard maternal diet in utero, but rats experiencing effects of high-fat diets in utero and during suckling showed the greatest body mass and highest blood pressure, as well as hyperinsulinism and hyperleptinemia as adults. The epigenetic processes that begin with maternal obesity have a greater impact on those who are already genetically susceptible to obesity.…”

Exposure of neonatal rats to maternal cafeteria feeding during suckling alters hepatic gene expression and DNA methylation in the insulin signalling pathway

“…However, in the Bayol study, insulin receptor expression was increased by cafeteria feeding at any stage of life in males and Irs2 was down-regulated by cafeteria diet in females. Effects of the diet on expression of PPARg and glucose transporters in adipose tissue were also reported (Bayol et al 2008). The differences between the current study and the work by Bayol and colleagues are most likely to be explained by variation in the nature of the cafeteria feeding regimens and different timing of exposure (control over litter size and variety of cafeteria foods offered).…”