Fig. 1: A maternal prenatal and perinatal high-fat diet (HFD) and metabolic disorder induce transient early-onset obesity, elevated adipocytokine levels, and impaired glucose tolerance in offspring.

A Animal model of metabolic programming. Female mice were fed a HFD for 7 weeks prior to mating; control mice received a standard diet (SD). The dams remained on their respective diets throughout gestation and lactation. The offspring of both groups were weaned at postnatal day 21 (P21) and fed SD until P70. B–D Body weight (B), body weight gain (C), and intraperitoneal glucose tolerance test (ipGTT) results (D) of dams prior to mating. E The body weight, ratio of epigonadal white adipose tissue (WAT) relative to body weight and mRNA expression of Il6 (interleukin-6) and Lep (leptin) in the WAT of offspring at P21 using qRT-PCR; HFD relative to SD. F Serum IL-6 and leptin concentrations in the offspring were assessed by ELISA at P21; offspring were subjected to the ipGTT. G The body weight, ratio of WAT relative to the body weight and expression of Il6 and Lep in the WAT of offspring at P70 using qRT-PCR; HFD relative to SD. H Serum IL-6 and leptin concentrations in the offspring at P70 using ELISA. Offspring were subjected to the ipGTT at P70. Data are shown as mean ± standard error of the mean B: SD n = 32, HFD n = 40; C SD n = 32, HFD n = 40; D SD n = 36, HFD n = 49; E SD n = 9–25, HFD n = 7–27; F SD n = 5–30, HFD n = 5–7; G SD n = 10–68, HFD n = 7–31; H SD n = 6–21, HFD n = 3–7. Statistical analyses were performed using the two-sided Mann–Whitney test, two-sided Student’s t test or two-way ANOVA followed by the Bonferroni post-test; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. Gray = standard diet; white = high-fat diet. A detailed list of sample sizes and P value per graph is provided in the Supplemental Material. Source data are provided as a Source Data file.