Evidence map›Paper›PMID 36914626›Full record

ArticleNature communications2023

De novo lipogenesis fuels adipocyte autophagosome and lysosome membrane dynamics.

Leslie A Rowland, Adilson Guilherme, Felipe Henriques, Chloe DiMarzio, Sean Munroe, Nicole Wetoska, Mark Kelly, Keith Reddig, Gregory Hendricks, Meixia Pan and 4 more

Open access · goldFull text read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
11.2field-weighted citation impact, top 1% of its field
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

24 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  8. PSD3 links autophagic flux to MHC-I-associated immune modulation in esophageal squamous cell carcinoma.Apoptosis : an international journal on programmed cell death · 2026
    Article
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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

14 authors at 3 institutions in 1 country.

Leslie A RowlandProgram in Molecular Medicine, University of Massachusetts Chan Medical School, Worcester, MA, 01605, USA. Leslie.rowland@umassmed.edu.ORCID 0000-0002-4497-2704
Adilson GuilhermeProgram in Molecular Medicine, University of Massachusetts Chan Medical School, Worcester, MA, 01605, USA.ORCID 0000-0003-0535-5911
Felipe HenriquesProgram in Molecular Medicine, University of Massachusetts Chan Medical School, Worcester, MA, 01605, USA.ORCID 0000-0002-9245-7141
Chloe DiMarzioProgram in Molecular Medicine, University of Massachusetts Chan Medical School, Worcester, MA, 01605, USA.
Sean MunroeProgram in Molecular Medicine, University of Massachusetts Chan Medical School, Worcester, MA, 01605, USA.
Nicole WetoskaProgram in Molecular Medicine, University of Massachusetts Chan Medical School, Worcester, MA, 01605, USA.
Mark KellyProgram in Molecular Medicine, University of Massachusetts Chan Medical School, Worcester, MA, 01605, USA.ORCID 0000-0001-9018-594X
Keith ReddigDepartment of Radiology, University of Massachusetts Chan Medical School, Worcester, MA, 01605, USA.
Gregory HendricksDepartment of Radiology, University of Massachusetts Chan Medical School, Worcester, MA, 01605, USA.
Meixia PanBarshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, USA.
Xianlin HanBarshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, USA.ORCID 0000-0002-8615-2413
Olga R IlkayevaDuke Molecular Physiology Institute, Department of Medicine, Division of Endocrinology, Metabolism and Nutrition, Duke University School of Medicine, Durham, NC, 27710, USA.ORCID 0000-0002-9779-0883
Christopher B NewgardDuke Molecular Physiology Institute, Department of Medicine, Division of Endocrinology, Metabolism and Nutrition, Duke University School of Medicine, Durham, NC, 27710, USA.ORCID 0000-0002-1293-691X
Michael P CzechProgram in Molecular Medicine, University of Massachusetts Chan Medical School, Worcester, MA, 01605, USA. Michael.Czech@umassmed.edu.ORCID 0000-0003-4075-7350
University of Massachusetts Chan Medical School · USDuke University · USThe University of Texas Health Science Center at San Antonio · US

Funding

TRANSGENIC COREP30AG013319 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI JAMES FLOYD NELSON · 1995 to 2026
$30.6M
San Antonio OAIC - Research Education Component (REC)P30AG044271 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Adam Salmon · 2015 to 2026
$14.1M
Pilot & Feasibility ProgramP30DK124723 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI P Darrell Neufer · 2020 to 2026
$11.0M
Insulin Signaling and Metabolic Regulation in AdipocytesR37DK030898 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1996 to 2021
$7.2M
Adipocyte to neuron signaling in thermogenic programming of white adipose tissueR01DK116056 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 2019 to 2023
$2.9M
Transmission Electron Microscope for Core EM FacilityS10OD025113 · OD · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HENDRICKS, GREGORY · 2018 to 2018
$600k
UltramicrotomeS10OD021580 · OD · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HENDRICKS, GREGORY · 2016 to 2016
$53k
NIA NIH HHS P30 AG013319NIA NIH HHS P30 AG044271NIDDK NIH HHS P30 DK124723NIDDK NIH HHS R01 DK116056NIDDK NIH HHS R37 DK030898NIH HHS S10 OD021580NIH HHS S10 OD025113
6 · The paper itself

Abstract

Adipocytes robustly synthesize fatty acids (FA) from carbohydrate through the de novo lipogenesis (DNL) pathway, yet surprisingly DNL contributes little to their abundant triglyceride stored in lipid droplets. This conundrum raises the hypothesis that adipocyte DNL instead enables membrane expansions to occur in processes like autophagy, which requires an abundant supply of phospholipids. We report here that adipocyte Fasn deficiency in vitro and in vivo markedly impairs autophagy, evident by autophagosome accumulation and severely compromised degradation of the autophagic substrate p62. Our data indicate the impairment occurs at the level of autophagosome-lysosome fusion, and indeed, loss of Fasn decreases certain membrane phosphoinositides necessary for autophagosome and lysosome maturation and fusion. Autophagy dependence on FA produced by Fasn is not fully alleviated by exogenous FA in cultured adipocytes, and interestingly, imaging studies reveal that Fasn colocalizes with nascent autophagosomes. Together, our studies identify DNL as a critical source of FAs to fuel autophagosome and lysosome maturation and fusion in adipocytes.

Indexed as

AutophagosomesLipogenesisAdipocytesAutophagyFatty AcidsLysosomesFatty Acids

Identifiers

PMID36914626
PMCPMC10011520
OpenAlexW4324129056

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read86
Read underepoch 390

Registered trials

None linked

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.