Summary of Study ST002754

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench,, where it has been assigned Project ID PR001715. The data can be accessed directly via it's Project DOI: 10.21228/M81D9R This work is supported by NIH grant, U2C- DK119886.


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Study IDST002754
Study TitleMetabolomics analysis of maternal obesity model
Study Summary100μl serum of 11-12 weeks old male mice with a background from various diet groups were processed in Metabolon ( for metabolics analysis.Diet groups are CDm CDl CD, CDm CDl HFD, CDmHFDl HFD, HFDm CDl CD, HFDm CDl HFD, HFDm HFDl CD and HFDm CDl CD. (m: maternal diet, l: lactation)
University of Bonn
LaboratoryMass Lab
Last NameMass
First NameElvira
AddressLIMES-Institute, Carl-Troll-Str. 31, 53115 Bonn, Germany
Phone+49 02 28 / 73 6 28 48
Submit Date2023-06-14
Num Groups6
Total Subjects42
Num Males42
Analysis Type DetailLC-MS
Release Date2023-08-01
Release Version1
Elvira Mass Elvira Mass application/zip

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Project ID:PR001715
Project DOI:doi: 10.21228/M81D9R
Project Title:Developmental programming of Kupffer cells by maternal obesity causes fatty liver disease in the offspring
Project Summary:Kupffer cells (KCs) are tissue-resident macrophages which colonize the developing liver early during embryogenesis. Throughout development and adulthood, KCs have distinct core functions that are essential for liver and organismal homeostasis, such as supporting fetal erythropoiesis as well as postnatal erythrocyte recycling and liver metabolism. KCs acquire their tissue-specific transcriptional signature immediately after colonizing the liver, mature together with the tissue, and adapt to the tissue’s function. However, whether perturbation of macrophage core functions during development may contribute to or cause disease at postnatal stages is poorly understood. Here, we utilize a maternal obesity model to disturb KC functions during gestation. We show that offspring born to obese mothers develop fatty liver disease that is accompanied by a local pro-inflammatory response, a phenotype that is augmented if the offspring is kept on control diet after birth. Further, transcriptional analyses reveal that KCs undergo developmental programming through the maternal high-fat diet, which lasts until adulthood. The offspring’s KC developmental programming is irreversible despite the switch to control diet and leads to increased lipid uptake in hepatocytes mediated via paracrine factors stemming from KCs. The transcriptional programming of KCs and the fatty liver disease phenotype are rescued by genetic depletion of hypoxia-inducible factor alpha (Hif-1alpha) in macrophages during gestation. These results demonstrate that macrophages rely on an undisturbed development to fulfil their core functions and support organ homeostasis during adulthood, and establish developmental programming of KCs as a therapeutic strategy for metabolic disorders, such as fatty liver disease.
Institute:University of Bonn
Laboratory:Mass Lab
Last Name:Mass
First Name:Elvira
Address:Carl-Troll-Str. 31, 53115 Bonn, Germany
Phone:+49 0228 / 73 6 28 48
Funding Source:DFG
Publications:in preparation
Contributors:Nora Balzer, Iva Splichalova, Hao Huang, Stephan Grein, Lea Seep