Evidence map›Paper›PMID 34686520›Full record

ArticleDiabetes2021

JMJD8 is a Novel Molecular Nexus Between Adipocyte-Intrinsic Inflammation and Insulin Resistance.

Dongjoo You, Byung Chul Jung, Sneha Damal Villivalam, Hee-Woong Lim, Sona Kang

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. JMJD8 facilitates hepatic lipid deposition and metabolic dysfunction.American journal of physiology. Endocrinology and metabolism · 2025
    Article
  3. Dietary Supplementation with Protocatechuic Acid and a ComplexAnimals : an open access journal from MDPI · 2025
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. JMJD8 Functions as a Novel AKT1 Lysine Demethylase.International journal of molecular sciences · 2022
    Article
  11. Article
  12. Article
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

5 authors at 2 institutions in 1 country.

Dongjoo YouNutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720.
Byung Chul JungNutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720.
Sneha Damal VillivalamNutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720.
Hee-Woong LimDivision of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, 3333 Burnet Ave. MLC 7024, Cincinnati, OH, 45229.
Sona KangNutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720 kangs@berkeley.edu.
University of California, Berkeley · USCincinnati Children's Hospital Medical Center · US

Funding

Stanford Islet Research CoreP30DK116074 · NIDDK · STANFORD UNIVERSITY · PI Seung K Kim · 2017 to 2026
$19.5M
Epigenetic regulation of adipose development and remodelingR01DK116008 · NIDDK · UNIVERSITY OF CALIFORNIA BERKELEY · PI Sona Kang · 2018 to 2026
$3.6M
NIDDK NIH HHS P30 DK116074NIDDK NIH HHS R01 DK116008
6 · The paper itself

Abstract

Chronic low-grade inflammation, often referred to as metainflammation, develops in response to overnutrition and is a major player in the regulation of insulin sensitivity. While many studies have investigated adipose tissue inflammation from the perspective of the immune cell compartment, little is known about how adipocytes intrinsically contribute to metainflammation and insulin resistance at the molecular level. Here, we demonstrate a novel role for Jumonji C Domain Containing Protein 8 (JMJD8) as an adipocyte-intrinsic molecular nexus between inflammation and insulin resistance. We determined that JMJD8 was highly enriched in white adipose tissue, especially in the adipocyte fraction. Adipose JMJD8 levels were dramatically increased in obesity-associated insulin resistance models. Its levels were increased by feeding and insulin, and inhibited by fasting. A JMJD8 gain of function was sufficient to drive insulin resistance, whereas loss of function improved insulin sensitivity in mouse and human adipocytes. Consistent with this,

Identifiers

PMID34686520
PMCPMC8763873
OpenAlexW3205660609

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.