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. 2015 Dec 25;5(3):184–197. doi: 10.1016/j.molmet.2015.12.002

Figure 2.

Figure 2

Impaired glucose tolerance and reduced body weight gain in response to HFD persists into two generations. (A–C) Metabolic profiling of F1 female offspring after 12 weeks of high fat feeding; blood (A) glucose and (B) insulin during an intraperitoneal glucose tolerance test (ipGTT) (n = 9–11 animals; 1 sibling per litter) and (C) body weight curve (n = 14–22 animals from 14 to 17 litters; used more than 1 sibling per litter). (D–F) Metabolic profiling of F2 female offspring after 12 weeks of high fat feeding: Blood (D) glucose and (E) insulin during an ipGTT (n = 5–6 litters; 1 sibling per litter) and (F) body weight curve (n = 10–13 animals from 5 to 6 litters; used more than one sibling per litter). Results are represented as mean ± SEM. Two-way ANOVA followed by Bonferroni post-hoc test: *p ≤ 0.05: PatCD-HF vs PatCD-CD or GpatCD-HF vs GpatCD-CD; ¤p ≤ 0.05: PatHF-CD vs PatCD-CD or GpatHF-CD vs GpatCD-CD; #p ≤ 0.05: PatHF-HF vs PatHF-CD or GpatHF-HF vs GpatHF-CD; +p ≤ 0.05: PatHF-HF vs PatCD-HF or GpatHF-HF vs GpatCD-HF. PatCD-CD: Paternal-Chow on Chow; PatHF-CD: Paternal-HFD on Chow; PatCD-HF: Paternal-Chow on HFD; PatHF-HF: Paternal-HFD on HFD; GpatCD-CD: Grandpaternal-Chow on Chow; GpatHF-CD: Grandpaternal-HFD on Chow; GpatCD-HF: Grandpaternal-Chow on HFD; GpatHF-HF: Grandpaternal-HFD on HFD.