Summary of Study ST002504
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001618. The data can be accessed directly via it's Project DOI: 10.21228/M8JT6D This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
| Study ID | ST002504 |
| Study Title | Lipid droplets and peroxisomes are co-regulated to drive lifespan extension in response to mono-unsaturated fatty acids |
| Study Summary | Dietary mono-unsaturated fatty acids (MUFAs) are linked to human longevity and extend lifespan in several species. But the mechanisms by which MUFAs extend lifespan remain unclear. Here we show that an organelle network involving lipid droplets and peroxisomes is critical for lifespan extension by MUFAs in C. elegans. MUFA accumulation increases lipid droplet number in fat storage tissues, and this is necessary for MUFA-induced longevity. Lipid droplet number in young or middle-aged individuals can predict remaining lifespan, consistent with a beneficial effect of lipid droplets on lifespan. Lipidomics datasets reveal that MUFA accumulation also modifies the ratio of membrane lipids and ether lipids, a signature predictive of decreased lipid oxidation. We validate that MUFAs decrease lipid oxidation in middle-aged individuals, and that this is important for MUFA-induced longevity. Intriguingly, the increase in lipid droplet number in response to MUFAs is accompanied by a concomitant increase in peroxisome number. Using a targeted screen, we identify genes involved in the co-regulation or uncoupling of this lipid droplet-peroxisome network. We find that induction of both organelles is optimal for lifespan extension. Our study uncovers an organelle network involved in lipid homeostasis and lifespan regulation and identifies a mechanism of action for MUFAs to extend lifespan, opening new avenues for lipid-based interventions to delay aging. For the manuscript only the conditions “control” and “ash-2 RNAi” are plotted |
| Institute | Stanford University |
| Last Name | Papsdorf |
| First Name | Katharina |
| Address | 290 Jane Stanford way, 94301 Palo Alto, CA, USA |
| papsdorf@stanford.edu | |
| Phone | +1 650 546 5366 |
| Submit Date | 2023-02-03 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | raw(Thermo) |
| Analysis Type Detail | LC-MS |
| Release Date | 2023-03-20 |
| Release Version | 1 |
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Collection:
| Collection ID: | CO002596 |
| Collection Summary: | At middle-age (adult day 5), worms were transferred to empty RNAi plates without any bacteria for 15 minutes, to clear residual bacteria in the gut. Worms were then collected in 200 µl M9 in protein-low bind Eppendorf tubes (cat # 13-698-794). Worms were lysed using a pre-chilled stainless-steel homogenizer (Wheaton, cat # 357572) and were homogenized with 15 plunger strokes and protein concentration of the lysate was determined using the Pierce BCA Protein Assay Kit (Thermo- Scientific). The lysate (from approximately 500 worms) was frozen on dry ice and stored at -80°C |
| Sample Type: | Whole worm lysate |
