Evidence map›Paper›PMID 32344065›Full record

ArticleMolecular metabolism2020

Adipocyte-specific Beclin1 deletion impairs lipolysis and mitochondrial integrity in adipose tissue.

Yeonho Son, Yoon Keun Cho, Abhirup Saha, Hyun-Jung Kwon, Ji-Hyun Park, Minsu Kim, Young-Suk Jung, Sang-Nam Kim, Cheoljun Choi, Je-Kyung Seong and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
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  6. Unraveling the Molecular Mechanisms of ABHD5 Membrane Targeting.bioRxiv : the preprint server for biology · 2025
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  15. mInternational journal of molecular sciences · 2022
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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

13 authors at 3 institutions in 3 countries.

Yeonho SonCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Republic of Korea.
Yoon Keun ChoCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Republic of Korea.
Abhirup SahaCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Republic of Korea.
Hyun-Jung KwonCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Republic of Korea.
Ji-Hyun ParkCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Republic of Korea.
Minsu KimCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Republic of Korea.
Young-Suk JungCollege of Pharmacy, Pusan National University, Busan, Republic of Korea.
Sang-Nam KimCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Republic of Korea.
Cheoljun ChoiCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Republic of Korea.
Je-Kyung SeongKorea Mouse Phenotyping Center (KMPC), Seoul National University, Seoul, Republic of Korea.
Rayanne B BurlCenter for Molecular Medicine and Genetics, Wayne State University, Detroit, MI, USA; Center for Integrative Metabolic and Endocrine Research, Wayne State University School of Medicine, Detroit, MI, USA.
James G GrannemanCenter for Molecular Medicine and Genetics, Wayne State University, Detroit, MI, USA; Center for Integrative Metabolic and Endocrine Research, Wayne State University School of Medicine, Detroit, MI, USA.
Yun-Hee LeeCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Republic of Korea. Electronic address: yunhee.lee@snu.ac.kr.
Seoul National University · KRWayne State University · USPusan National University · KR

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Scott Soleimanpour · 2013 to 2026
$24.3M
Analysis of Cellular Plasticity in White Adipose Tissue.R01DK062292 · NIDDK · WAYNE STATE UNIVERSITY · PI James G Granneman · 2003 to 2026
$7.6M
Deconstructing the brown neogenic zone in classic brown adipose tissueF31DK116536 · NIDDK · WAYNE STATE UNIVERSITY · PI BURL, RAYANNE · 2018 to 2020
$112k
NIDDK NIH HHS F31 DK116536NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK062292
6 · The paper itself

Abstract

objectiveBeclin1 is a core molecule of the macroautophagy machinery. Although dysregulation of macroautophagy is known to be involved in metabolic disorders, the function of Beclin1 in adipocyte metabolism has not been investigated. In the present study, we aimed to study the role of Beclin1 in lipolysis and mitochondrial homeostasis of adipocytes.

methodsAutophagic flux during lipolysis was examined in adipocytes cultured in vitro and in the adipose tissue of mice. Adipocyte-specific Beclin1 knockout (KO) mice were used to investigate the activities of Beclin1 in adipose tissues.

resultscAMP/PKA signaling increased the autophagic flux in adipocytes differentiated from C3H10T1/2 cells. In vivo autophagic flux was higher in the brown adipose tissue (BAT) than that in the white adipose tissue and was further increased by the β3 adrenergic receptor agonist CL316243. In addition, surgical denervation of BAT greatly reduced autophagic flux, indicating that sympathetic nerve activity is a major regulator of tissue autophagy. Adipocyte-specific KO of Beclin1 led to a hypertrophic enlargement of lipid droplets in BAT and impaired CL316243-induced lipolysis/lipid mobilization and energy expenditure. While short-term effects of Beclin1 deletion were characterized by an increase in mitochondrial proteins, long-term Beclin1 deletion led to severe disruption of autophagy, resulting in mitochondrial loss, and dramatically reduced the expression of genes involved in lipid metabolism. Consequently, adipose tissue underwent increased activation of cell death signaling pathways, macrophage recruitment, and inflammation, particularly in BAT.

conclusionsThe present study demonstrates the critical roles of Beclin1 in the maintenance of lipid metabolism and mitochondrial homeostasis in adipose tissues.

Indexed as

Gene DeletionAdipocytesAdipose TissueAdipose Tissue, BrownAnimalsAutophagyBeclin-1Cell LineCyclic AMPCyclic AMP-Dependent Protein KinasesDNA Copy Number VariationsImmunityLipid MetabolismLipolysisMiceMice, KnockoutBeclin-1Cyclic AMPCyclic AMP-Dependent Protein KinasesMitochondrial ProteinsReceptors, Adrenergic, beta-3Beclin1Brown adipose tissueLipolysisLipophagyMitophagyWhite adipose tissue

Identifiers

PMID32344065
PMCPMC7235646
OpenAlexW3018379706

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.