Fig. 6. Iron supplementation potentiates embryonic malformation and placental apoptosis in a mouse model of Western diet-induced obesity.

a Starting at 3 weeks of age, wild-type C57BL/6 (iron-adequate) or hepcidin KO (genetic iron overload, dark blue circles) females were fed an iron-adequate Western diet (100 ppm iron) for 8 weeks. After 8 weeks, half of the WT mice were switched to a high-iron Western diet (3700 ppm carbonyl iron, dietary iron loading, light blue circles) for 1–3 weeks, while the other mice continued on the iron-adequate Western diet (gray circles). Mice were mated and continued their respective diets during pregnancy. Iron adequate dams were compared to dietary or genetic iron-loaded dams. b Weight of female mice at mating fed a Western diet compared to those fed non-obesogenic diet. c Incidence of E18.5 embryos with adverse outcomes in obese pregnancies. d Embryo gross morphology and e incidence of embryos with subcutaneous hemorrhaging or f malformations. g Incidence of embryo malformations categorized by type. Incidence of embryo h anophthalmia and i microphthalmia. j Western blot (left) and quantitation (right) of cleaved caspase-3 in whole placentas normalized to β-actin. Representative blot of n = 11–14 randomly selected placentas/group. b, c, e, f, h–j Error bars represent mean ± s.e.m. Statistical differences were determined by two-tailed Student’s t-test (denoted by *), one-way ANOVA on ranks followed by Dunn’s method for multiple comparisons (denoted by #), or Fisher’s exact test (indicated by ‡). P-values are indicated in each figure panel. Source data are provided as a Source data file.