Figure 6.

Offspring hypothalamic appetite signaling in peripubertal mice, following maternal HFHC-diet-induced obesity. Hypothalamic gene expression of insulin receptor (A), melanocortin 4 receptor (C), leptin receptor (D), neuropeptide-Y (gene transcript for hunger neuropeptide, E), proopiomelanocortin (gene transcript for satiety neuropeptide, F), glucocorticoid receptor (G), corticotropin-releasing hormone (H), and estrogen receptor alpha (I) were measured in fasted offspring, following weaning from CON and HFHC dams. There were no significant differences between CON and HFHC groups in the male or female offspring studied separately. There was an interaction between diet and sex in insulin receptor (B) such that males had a lower insulin receptor expression and the females had higher insulin receptor expression, when exposed to maternal HFHC diet (B, p = 0.03). The HFHC offspring had a lower glucocorticoid receptor expression (C, p = 0.05) compared to the CON offspring. The female offspring had a higher glucocorticoid receptor (C, p < 0.0001), NPY (D, p < 0.001), POMC (E, p = 0.001), and CRH (F, p = 0.004), compared to the male offspring. Results are expressed as mean ± SEM. CON—offspring born to dams maintained on control diet; HFHC—offspring born to dams maintained on high-fat–high-carbohydrate diet; black line (B) represents maternal CON-diet-exposed offspring; red line (B) represents maternal HFHC-diet-exposed offspring. NPY—neuropeptide-Y; POMC—proopiomelanocortin; CRH—corticotropin-releasing hormone. Open bars represent CON offspring; closed bars represent HFHC offspring; unpaired t-test or two-way ANOVA, followed by post-hoc Tukey’s HSD, n = 7–13/group, vs. offspring born to dams consuming same diet (diet effect), vs. male offspring born to dams consuming different diets (sex effect); * p < 0.05, p values > 0.1 were recorded as non-significant (NS).