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-gamma (PPARgamma), 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.

Figures

Figure 1. Serum biochemistry

Circulating glucose, insulin, triglyceride and cholesterol levels in male (M) and female (F) rat offspring from the various dietary groups. Keys: open bar: CCC group, chow throughout; lightly shaded bar: CCJ group, chow in pregnancy and lactation followed by junk food diet after weaning; darkly shaded bar: JJC group, junk food diet in pregnancy and lactation followed by chow after weaning; black bar: JJJ group, junk food diet throughout. Results are mean ± s.e.m. Different letters indicate statistical differences (P < 0.05) by hierarchical two-way ANOVA followed by post hoc analyses with n = 18 males and n = 18 females in each nutritional group.

Figure 2. Histological data

Perirenal fat pad mass, perirenal fat pad mass relative to body weight (BW), average adipocyte area and (adipocyte area × fat pad mass) in male (M) and female (F) offspring from the various dietary groups. Keys: open bar: CCC group, chow throughout; lightly shaded bar: CCJ group, chow in pregnancy and lactation followed by junk food diet after weaning; darkly shaded bar: JJC group, junk food diet in pregnancy and lactation followed by chow after weaning; black bar: JJJ group, junk food diet throughout. Results are mean ± s.e.m. Different letters indicate statistical differences (P < 0.05) by hierarchical two-way ANOVA followed by post hoc analyses with n = 18 males and n = 18 females in each nutritional group.

Figure 3. Transcriptional analysis of genes that regulate adipocyte proliferation, differentiation and growth

Real-time PCR analysis of IGF-1, IRS-1, VEGF-A and PPARγ mRNA expression in male (M) and female (F) offspring from the various dietary groups. Keys: open bar: CCC group, chow throughout; lightly shaded bar: CCJ group, chow in pregnancy and lactation followed by junk food diet after weaning; darkly shaded bar: JJC group, junk food diet in pregnancy and lactation followed by chow after weaning; black bar: JJJ group, junk food diet throughout. Results are mean ± s.e.m. Different letters indicate statistical differences (P < 0.05) by hierarchical two-way ANOVA followed by post hoc analyses with n = 18 males and n = 18 females in each nutritional group.

Figure 4. Transcriptional analysis of adipokines and adipsin

Real-time PCR analysis of leptin, adipsin and adiponectin mRNA expression in male (M) and female (F) offspring from the various dietary groups. Keys: open bar: CCC group, chow throughout; lightly shaded bar: CCJ group, chow in pregnancy and lactation followed by junk food diet after weaning; darkly shaded bar: JJC group, junk food diet in pregnancy and lactation followed by chow after weaning; black bar: JJJ group, junk food diet throughout. Results are mean ± s.e.m. Different letters indicate statistical differences (P < 0.05) by hierarchical two-way ANOVA followed by post hoc analyses with n = 18 males and n = 18 females in each nutritional group.

Figure 5. Transcriptional analysis of genes that regulate glucose and lipid transport

Real-time PCR analysis of Glut 1, Glut 3, Glut 4 and LPL mRNA expression in male (M) and female (F) offspring from the various dietary groups. Keys: open bar: CCC group, chow throughout; lightly shaded bar: CCJ group, chow in pregnancy and lactation followed by junk food diet after weaning; darkly shaded bar: JJC group, junk food diet in pregnancy and lactation followed by chow after weaning; black bar: JJJ group, junk food diet throughout. Results are mean ± s.e.m. Different letters indicate statistical differences (P < 0.05) by hierarchical two-way ANOVA followed by post hoc analyses with n = 18 males and n = 18 females in each nutritional group.