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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Treatment:
| Treatment ID: | TR002615 |
| Treatment Summary: | Hermaphrodites were treated with control (empty vector) RNAi, prx-5, ash-2 or prx-5/ash-2 RNAi until middle-age (adult day 6). Each condition consists of six biological replicates. To retrieve a large number of age-synchronized worms, approximately 500 eggs were laid by age-synchronized adult day 1 wild type parents per replicate plate. After 2 hours of egg laying, the parents were removed, and the plates were checked that no parents remained. Once the worms reached the young adult stage, they were washed each day to separate the adult worms from larvae/eggs. For this, worms were collected in M9 buffer (22 mM KH2PO4, 34 mM K2HPO4, 86 mM NaCl, 1mM MgSO4) and allowed to settle to the bottom of the tube. The supernatant was removed and fresh M9 was added. This washing procedure was repeated 6 times and the adult worms were transferred to fresh 6-cm RNAi plates seeded with 500 µl RNAi-expressing HT115 bacteria. |
