Image data related to the publication "Kupffer cell programming by maternal obesity triggers fatty liver disease"

Upon liver colonization, KCs rapidly acquire a tissue-specific transcriptional signature, mature alongside the developing liver, and adapt to its functions. Throughout development and adulthood, KCs perform distinct core functions essential for liver and organismal homeostasis, including supporting fetal erythropoiesis, postnatal erythrocyte recycling, and liver metabolism.

However, whether perturbations of macrophage core functions during development contribute to or cause disease at postnatal stages is poorly understood. Here, we utilize a mouse model of maternal obesity to perturb KC functions during gestation. We show that offspring exposed to maternal obesity develop fatty liver disease, driven by aberrant developmental programming of KCs that persists into adulthood.