Fig. 2

First-generation adult PNE offspring do not develop adiposity or type 2 diabetes. a Cumulative food intake of PNE offspring and control offspring (in kcal) was determined after 16 weeks of diet. b Monthly body weight measurements concomitant with body composition measurements. c–e Relative body fat (c), relative lean mass (d), and relative fluid mass (e) in % of body weight (BW) determined monthly by nuclear magnetic resonance. f–l metabolic cage measurements of 24-h food intake (FI) (f), 24-h energy expenditure (EE) (g), 24-h oxygen consumption rates (VO₂) (h), 24-h carbon dioxide production rates (VCO₂) (i), respiratory exchange ratio (RER) (j), and 24-h locomotor activity (k, l) in week 10 of the diets. EE, VO₂, and VCO₂ were normalized to the lean mass determined by nuclear magnetic resonance prior to the start of the measurements. Locomotor activity was measured as horizontal (k) and vertical beam breaks counts (l). m Fasting glucose. n Fasting insulin determined in week 16 of the diets. o–p Area under the curve (AUC) determination of Glucose tolerance tests (GTT) conducted in week 6 of the diet (o) and Insulin tolerance tests (ITT) conducted in week 10 of the diets (p). q–r, Glucose concentration measurements during the GTT (q) and ITT (r). Mice were injected i.p. glucose 1 g/kg (q) or Insulin 0.5 IU/kg (r). Data were analyzed by two-way ANOVA (a–p) or two-way RM ANOVA (q, r) followed by Bonferroni post-tests (*, p < 0.05; **, p < 0.01; ***, p < 0.001) or by t test (f) (^#, p < 0.05). The number of male offspring in each group was n = 5–9 originating from at least three different dams. All data are expressed as mean ± SEM. HFD intake effectively rendered mice obese, diabetic and hypoactive (a–i, k–p: p < 0.005, HFD vs. STD, two-way ANOVA)