Evidence map›Paper›PMID 37977245›Full record

ReviewJournal of hepatology2024

Pharmacologic inhibition of lipogenesis for the treatment of NAFLD.

William P Esler, David E Cohen

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of hepatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
18.5field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Review
  7. Zfp217 Regulates Hepatic de Novo Lipogenesis via METTL3-Mediated N6-Methyladenosine Modification of SREBF1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Frontiers in nutrition · 2026
    Article
  20. Article

2 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

William P EslerInternal Medicine Research Unit, Pfizer Worldwide Research Development and Medical, Cambridge, MA 02139 United States. Electronic address: william.esler@pfizer.com.
David E CohenDivision of Gastroenterology, Hepatology and Endoscopy, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115 United States. Electronic address: dcohen@bwh.harvard.edu.
Brigham and Women's Hospital · USPfizer (United States) · US

Funding

Phospholipid-Mediated Metabolic Control in the Pathogenesis of NAFLDR01DK056626 · NIDDK · YESHIVA UNIVERSITY · PI COHEN, DAVID E. · 2000 to 2024
$10.3M
Them1-Mediated Metabolic Regulation and Pathogenic Role in NAFLDR01DK103046 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI DAVID E. COHEN, Susan J Hagen · 2015 to 2026
$7.6M
Regulation of Hepatic Lipid and Glucose Metabolism by Phosphatidylcholine TransfeR01DK048873 · NIDDK · YESHIVA UNIVERSITY · PI DAVID E. COHEN · 2003 to 2026
$5.8M
Regulation of Hepatic Lipid and Glucose Metabolism by PC-TP/StarD2R37DK048873 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI COHEN, DAVID E. · 2012 to 2021
$5.5M
Them1 Inhibitors for the Management of Non-Alcoholic Fatty Liver DiseaseR01DK133988 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI DAVID E. COHEN · 2023 to 2026
$2.0M
NIDDK NIH HHS R01 DK048873NIDDK NIH HHS R01 DK056626NIDDK NIH HHS R01 DK103046NIDDK NIH HHS R01 DK133988NIDDK NIH HHS R37 DK048873
6 · The paper itself

Abstract

The hepatic accumulation of excess triglycerides is a seminal event in the initiation and progression of non-alcoholic fatty liver disease (NAFLD). Hepatic steatosis occurs when the hepatic accrual of fatty acids from the plasma and de novo lipogenesis (DNL) is no longer balanced by rates of fatty acid oxidation and secretion of very low-density lipoprotein-triglycerides. Accumulating data indicate that increased rates of DNL are central to the development of hepatic steatosis in NAFLD. Whereas the main drivers in NAFLD are transcriptional, owing to both hyperinsulinemia and hyperglycaemia, the effectors of DNL are a series of well-characterised enzymes. Several have proven amenable to pharmacologic inhibition or oligonucleotide-mediated knockdown, with lead compounds showing liver fat-lowering efficacy in phase II clinical trials. In humans with NAFLD, percent reductions in liver fat have closely mirrored percent inhibition of DNL, thereby affirming the critical contributions of DNL to NAFLD pathogenesis. The safety profiles of these compounds have so far been encouraging. It is anticipated that inhibitors of DNL, when administered alone or in combination with other therapeutic agents, will become important agents in the management of human NAFLD.

Indexed as

Non-alcoholic Fatty Liver DiseaseHumansLipid MetabolismLipogenesisLiverTriglyceridesTriglyceridesDNLLipogenesisNASHsteatosis

Identifiers

PMID37977245
PMCPMC10842769
OpenAlexW4388694639

What OpenQuestion holds

Textmetadata
LicenceTDM
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.