Evidence map›Paper›PMID 32475074›Full record

ArticleAging cell2020

Caenorhabditis elegans Lipin 1 moderates the lifespan-shortening effects of dietary glucose by maintaining ω-6 polyunsaturated fatty acids.

Yoonji Jung, Sujeong Kwon, Seokjin Ham, Dongyeop Lee, Hae-Eun H Park, Yasuyo Yamaoka, Dae-Eun Jeong, Murat Artan, Ozlem Altintas, Sangsoon Park and 7 more

Abstract read
In one paragraph

Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed.

  1. Article
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  8. Arachidonic acid in aging: New roles for old players.Journal of advanced research · 2025
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Yoonji JungDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.
Sujeong KwonDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.
Seokjin HamDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.ORCID 0000-0002-6950-2848
Dongyeop LeeDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, South Korea.
Hae-Eun H ParkDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.
Yasuyo YamaokaDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, South Korea.
Dae-Eun JeongDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, South Korea.
Murat ArtanDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, South Korea.
Ozlem AltintasSchool of Interdisciplinary Bioscience and Bioengineering, Pohang University of Science and Technology, Pohang, South Korea.
Sangsoon ParkDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, South Korea.ORCID 0000-0002-5008-1609
Wooseon HwangDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, South Korea.
Yujin LeeDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.
Heehwa G SonDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.
Seon Woo A AnDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.
Eun Ji E KimDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.
Mihwa SeoDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, South Korea.
Seung-Jae V LeeDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, South Korea.ORCID 0000-0002-6103-156X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive glucose causes various diseases and decreases lifespan by altering metabolic processes, but underlying mechanisms remain incompletely understood. Here, we show that Lipin 1/LPIN-1, a phosphatidic acid phosphatase and a putative transcriptional coregulator, prevents life-shortening effects of dietary glucose on Caenorhabditis elegans. We found that depletion of lpin-1 decreased overall lipid levels, despite increasing the expression of genes that promote fat synthesis and desaturation, and downregulation of lipolysis. We then showed that knockdown of lpin-1 altered the composition of various fatty acids in the opposite direction of dietary glucose. In particular, the levels of two ω-6 polyunsaturated fatty acids (PUFAs), linoleic acid and arachidonic acid, were increased by knockdown of lpin-1 but decreased by glucose feeding. Importantly, these ω-6 PUFAs attenuated the short lifespan of glucose-fed lpin-1-inhibited animals. Thus, the production of ω-6 PUFAs is crucial for protecting animals from living very short under glucose-rich conditions.

Indexed as

AnimalsCaenorhabditis elegansDietFatty Acids, UnsaturatedGlucoseHumansPhosphatidate PhosphataseFatty Acids, UnsaturatedGlucoseLPIN1 protein, humanPhosphatidate PhosphataseagingC. elegansglucoseLPIN-1metabolismω-6 polyunsaturated fatty acids

Identifiers

PMID32475074
PMCPMC7294780

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.