Evidence map›Paper›PMID 33836591›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

DNMT1 maintains metabolic fitness of adipocytes through acting as an epigenetic safeguard of mitochondrial dynamics.

Yoon Jeong Park, Sangseon Lee, Sangsoo Lim, Hahn Nahmgoong, Yul Ji, Jin Young Huh, Assim A Alfadda, Sun Kim, Jae Bum Kim

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 43 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Yoon Jeong ParkNational Creative Research Initiatives Center for Adipocyte Structure and Function, Seoul National University, Seoul 08826, South Korea.
Sangseon LeeBioinformatics Institute, Seoul National University, Seoul 08826, South Korea.ORCID 0000-0002-7398-9580
Sangsoo LimBioinformatics Institute, Seoul National University, Seoul 08826, South Korea.
Hahn NahmgoongNational Creative Research Initiatives Center for Adipocyte Structure and Function, Seoul National University, Seoul 08826, South Korea.
Yul JiNational Creative Research Initiatives Center for Adipocyte Structure and Function, Seoul National University, Seoul 08826, South Korea.
Jin Young HuhNational Creative Research Initiatives Center for Adipocyte Structure and Function, Seoul National University, Seoul 08826, South Korea.ORCID 0000-0002-0980-7199
Assim A AlfaddaObesity Research Center, College of Medicine, King Saud University, Riyadh, 11461, Saudi Arabia.ORCID 0000-0002-4792-5188
Sun KimBioinformatics Institute, Seoul National University, Seoul 08826, South Korea.
Jae Bum KimNational Creative Research Initiatives Center for Adipocyte Structure and Function, Seoul National University, Seoul 08826, South Korea; jaebkim@snu.ac.kr.
Seoul National University · KRKing Saud University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

White adipose tissue (WAT) is a key regulator of systemic energy metabolism, and impaired WAT plasticity characterized by enlargement of preexisting adipocytes associates with WAT dysfunction, obesity, and metabolic complications. However, the mechanisms that retain proper adipose tissue plasticity required for metabolic fitness are unclear. Here, we comprehensively showed that adipocyte-specific DNA methylation, manifested in enhancers and CTCF sites, directs distal enhancer-mediated transcriptomic features required to conserve metabolic functions of white adipocytes. Particularly, genetic ablation of adipocyte Dnmt1, the major methylation writer, led to increased adiposity characterized by increased adipocyte hypertrophy along with reduced expansion of adipocyte precursors (APs). These effects of Dnmt1 deficiency provoked systemic hyperlipidemia and impaired energy metabolism both in lean and obese mice. Mechanistically, Dnmt1 deficiency abrogated mitochondrial bioenergetics by inhibiting mitochondrial fission and promoted aberrant lipid metabolism in adipocytes, rendering adipocyte hypertrophy and WAT dysfunction. Dnmt1-dependent DNA methylation prevented aberrant CTCF binding and, in turn, sustained the proper chromosome architecture to permit interactions between enhancer and dynamin-1-like protein gene

Indexed as

Epigenesis, GeneticMitochondrial DynamicsAdipocytesAdipose TissueAdiposityAnimalsCCCTC-Binding FactorChromosome StructuresDNA (Cytosine-5-)-Methyltransferase 1DNA MethylationDynaminsEnergy MetabolismEnhancer Elements, GeneticGene Expression ProfilingLipid MetabolismMiceCCCTC-Binding FactorCtcf protein, mouseDNA (Cytosine-5-)-Methyltransferase 1Dnm1l protein, mouseDnmt1 protein, mouseDynaminsadipositychromosome structureDNA methylationmetabolic diseasemitochondria

Identifiers

PMID33836591
PMCPMC7980432
OpenAlexW3135208977

What OpenQuestion holds

Textmetadata
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.