Evidence map›Paper›PMID 33440156›Full record

ArticleCell reports2021

Endogenous Fatty Acid Synthesis Drives Brown Adipose Tissue Involution.

Christian Schlein, Alexander W Fischer, Frederike Sass, Anna Worthmann, Klaus Tödter, Michelle Y Jaeckstein, Janina Behrens, Matthew D Lynes, Michael A Kiebish, Niven R Narain and 11 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 53 citations in OpenAlex.

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  15. What defines a cell type? Perspectives from adipocyte biology.International journal of obesity (2005) · 2025
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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

21 authors at 5 institutions in 3 countries.

Christian SchleinDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Alexander W FischerDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Frederike SassDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Anna WorthmannDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Klaus TödterDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Michelle Y JaecksteinDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Janina BehrensDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Matthew D LynesSection on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.
Michael A KiebishBERG, Framingham, MA, USA.
Niven R NarainBERG, Framingham, MA, USA.
Val BussbergBERG, Framingham, MA, USA.
Abena DarkwahBERG, Framingham, MA, USA.
Naja Zenius JespersenCentre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Søren NielsenCentre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Camilla ScheeleCentre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark; Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.
Michaela SchweizerCore Facility of Electron Microscopy, Center for Molecular Neurobiology ZMNH, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Ingke BrarenVector Facility, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Alexander BarteltDepartment of Molecular Metabolism & Sabri Ülker Center, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University, 81377 Munich, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany; Institute for Diabetes and Cancer (IDC), Helmholtz Center Munich, Neuherberg, Germany.
Yu-Hua TsengSection on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA, USA.
Joerg HeerenDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Ludger SchejaDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Electronic address: l.scheja@uke.de.
Universität Hamburg · DEFramingham State University · USUniversity of Copenhagen · DKJoslin Diabetes Center · USGerman Centre for Cardiovascular Research · DE

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI JEAN E. SCHAFFER · 1986 to 2026
$50.5M
The Lipidomics of Adipose Tissue ThermogenesisK01DK111714 · NIDDK · MAINEHEALTH · PI LYNES, MATTHEW D · 2017 to 2021
$804k
Telomerase as a Marker of Brown and White Adipose Tissue Stem CellsF32DK102320 · NIDDK · JOSLIN DIABETES CENTER · PI LYNES, MATTHEW D · 2014 to 2014
$53k
NIDDK NIH HHS F32 DK102320NIDDK NIH HHS K01 DK111714NIDDK NIH HHS P30 DK036836
6 · The paper itself

Abstract

Thermoneutral conditions typical for standard human living environments result in brown adipose tissue (BAT) involution, characterized by decreased mitochondrial mass and increased lipid deposition. Low BAT activity is associated with poor metabolic health, and BAT reactivation may confer therapeutic potential. However, the molecular drivers of this BAT adaptive process in response to thermoneutrality remain enigmatic. Using metabolic and lipidomic approaches, we show that endogenous fatty acid synthesis, regulated by carbohydrate-response element-binding protein (ChREBP), is the central regulator of BAT involution. By transcriptional control of lipogenesis-related enzymes, ChREBP determines the abundance and composition of both storage and membrane lipids known to regulate organelle turnover and function. Notably, ChREBP deficiency and pharmacological inhibition of lipogenesis during thermoneutral adaptation preserved mitochondrial mass and thermogenic capacity of BAT independently of mitochondrial biogenesis. In conclusion, we establish lipogenesis as a potential therapeutic target to prevent loss of BAT thermogenic capacity as seen in adult humans.

Indexed as

Adipose Tissue, BrownAnimalsFatty AcidsHumansMiceFatty Acidsbrown adipose tissuecardiolipinsChREBPde novo lipogenesisenergy expenditurefatty acidsfatty acid synthesislipidomemitochondriamitophagynon-shivering thermogenesisphospholipidsthermoneutralitytriacylglycerolswhitening

Identifiers

PMID33440156
PMCPMC8240962
OpenAlexW3120360532

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.