Evidence map›Paper›PMID 37782317›Full record

ArticleeLife2023

Mice lacking triglyceride synthesis enzymes in adipose tissue are resistant to diet-induced obesity.

Chandramohan Chitraju, Alexander W Fischer, Yohannes A Ambaw, Kun Wang, Bo Yuan, Sheng Hui, Tobias C Walther, Robert V Farese

Open access · goldAbstract read
In one paragraph

Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Essential Biology of Lipid Droplets.Annual review of biochemistry · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. DIDO is necessary for the adipogenesis that promotes diet-induced obesity.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. Article
  14. 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

8 authors at 3 institutions in 1 country.

Chandramohan ChitrajuDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, United States.ORCID 0000-0001-8338-8976
Alexander W FischerDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, United States.ORCID 0000-0001-6717-9090
Yohannes A AmbawDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, United States.
Kun WangDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, United States.
Bo YuanDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, United States.
Sheng HuiDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, United States.
Tobias C Walther *Department of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, United States.ORCID 0000-0003-1442-1327
Robert V Farese *Department of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, United States.ORCID 0000-0001-8103-2239
Harvard University · USBroad Institute · USMemorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Mechanisms of Lipid Droplet FormationR01GM124348 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI FARESE, ROBERT V · 2017 to 2024
$2.9M
Howard Hughes Medical InstituteNCI NIH HHS P30 CA008748NIGMS NIH HHS R01 GM124348
6 · The paper itself

Abstract

Triglycerides (TGs) in adipocytes provide the major stores of metabolic energy in the body. Optimal amounts of TG stores are desirable as insufficient capacity to store TG, as in lipodystrophy, or exceeding the capacity for storage, as in obesity, results in metabolic disease. We hypothesized that mice lacking TG storage in adipocytes would result in excess TG storage in cell types other than adipocytes and severe lipotoxicity accompanied by metabolic disease. To test this hypothesis, we selectively deleted both TG synthesis enzymes, DGAT1 and DGAT2, in adipocytes (ADGAT DKO mice). As expected with depleted energy stores, ADGAT DKO mice did not tolerate fasting well and, with prolonged fasting, entered torpor. However, ADGAT DKO mice were unexpectedly otherwise metabolically healthy and did not accumulate TGs ectopically or develop associated metabolic perturbations, even when fed a high-fat diet. The favorable metabolic phenotype resulted from activation of energy expenditure, in part via BAT (brown adipose tissue) activation and beiging of white adipose tissue. Thus, the ADGAT DKO mice provide a fascinating new model to study the coupling of metabolic energy storage to energy expenditure.

Indexed as

AdipocytesObesityAdipose Tissue, BrownAnimalsDiet, High-FatMiceTriglyceridesTriglyceridesadipose tissuefatglucose metabolismlipodystrophymedicinemetabolismmousetriglyceride

Identifiers

PMID37782317
PMCPMC10545428
OpenAlexW4376141546

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.