Summary of Study ST002184

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 PR001391. The data can be accessed directly via it's Project DOI: 10.21228/M8X99S This work is supported by NIH grant, U2C- DK119886.


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Study IDST002184
Study TitleMetabolic effect of the loss of mitochondrial-specific aspartyl-tRNA synthetase Das2 on mouse intestinal epithelial cells
Study SummaryWe analysed the intestinal epithelial cell (IEC) from Dars2 fl/fl ; VillinCreERT2 tg/wt mice (n=15) and and Dars2 fl/fl ; VillinCreERT2 wt/wt mice (n=9) at 8 days upon tamoxifen injection to assess the metabolic effect of Das2 loss. Isolated IECs were divided into three technical replicates (n=69) and analysed with two analytical repeats (n=138).
CECAD Research Center
Last NameYang
First NameMing
AddressJoseph-Stelzmann-Straße 26, Köln, Koeln, 50931, Germany
Submit Date2022-06-01
Raw Data AvailableYes
Raw Data File Type(s)raw(Thermo)
Analysis Type DetailLC-MS
Release Date2022-06-15
Release Version1
Ming Yang Ming Yang application/zip

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Project ID:PR001391
Project DOI:doi: 10.21228/M8X99S
Project Title:Mitochondria regulate dietary lipid processing in enterocytes
Project Summary:Digested dietary fats are taken up, processed and transported by enterocytes to supply the body with lipids. Most absorbed lipids are assembled into pre-chylomicrons in the endoplasmic reticulum (ER) of enterocytes, which are then transported to the Golgi for maturation and subsequent secretion to the circulation. The role of mitochondria in regulating intestinal lipid transport remains unknown. Here we show that mitochondrial dysfunction in enterocytes inhibits chylomicron production and the transport of dietary lipids to peripheral organs. Mice with intestinal epithelial cell (IEC)-specific ablation of the mitochondrial-specific aspartyl - tRNA synthetase DARS2, as well as of the respiratory chain subunit SDHA or the assembly factor COX10 failed to thrive and showed massive accumulation of lipids within large lipid droplets (LDs) in enterocytes of the proximal small intestine (SI). Feeding a fat-free diet inhibited the formation of LDs in DARS2-deficient enterocytes, showing that accumulating lipids derive mostly from digested fat. Furthermore, metabolic tracing studies revealed impaired transport of dietary lipids to peripheral organs in mice lacking DARS2 in IECs. Moreover, DARS2-deficient enterocytes showed a distinct lack of mature chylomicrons concomitant with a disorganisation of the Golgi apparatus, suggesting that impaired ER to Golgi trafficking underlies impaired chylomicron production and secretion. Taken together, these results revealed a vital role of mitochondria in regulating dietary lipid transport in enterocytes, which is relevant for understanding the intestinal and nutritional defects observed in patients with mitochondrial defects.
Institute:CECAD Research Center
Last Name:Yang
First Name:Ming
Address:Joseph-Stelzmann-Straße 26, Köln, Koeln, 50931, Germany