Evidence map›Paper›PMID 41321937›Full record

ArticleJHEP reports : innovation in hepatology2025

Adipose microsomal triglyceride transfer protein deficiency protects against hepatic steatosis by upregulating PPARα activity.

Sujith Rajan, Michael Verano, Thomas Palaia, Chandana Prakashmurthy, Jay Chung, Shahidul Islam, Lili Lee, Antonisamy William James, José O Alemán, Ira J Goldberg and 2 more

Abstract read
In one paragraph

Article in JHEP reports : innovation in hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Review
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

12 authors.

Sujith RajanDepartment of Foundations of Medicine, NYU Grossman Long Island School of Medicine, and Diabetes and Obesity Research Center, NYU Langone Hospitals - Long Island, Mineola, NY, USA.
Michael VeranoHolman Division of Endocrinology, Department of Medicine, NYU Grossman School of Medicine, NY, USA.
Thomas PalaiaDepartment of Foundations of Medicine, NYU Grossman Long Island School of Medicine, and Diabetes and Obesity Research Center, NYU Langone Hospitals - Long Island, Mineola, NY, USA.
Chandana PrakashmurthyDepartment of Foundations of Medicine, NYU Grossman Long Island School of Medicine, and Diabetes and Obesity Research Center, NYU Langone Hospitals - Long Island, Mineola, NY, USA.
Jay ChungDepartment of Foundations of Medicine, NYU Grossman Long Island School of Medicine, and Diabetes and Obesity Research Center, NYU Langone Hospitals - Long Island, Mineola, NY, USA.
Shahidul IslamDepartment of Foundations of Medicine, NYU Grossman Long Island School of Medicine, and Diabetes and Obesity Research Center, NYU Langone Hospitals - Long Island, Mineola, NY, USA.
Lili LeeHolman Division of Endocrinology, Department of Medicine, NYU Grossman School of Medicine, NY, USA.
Antonisamy William JamesDepartment of Foundations of Medicine, NYU Grossman Long Island School of Medicine, and Diabetes and Obesity Research Center, NYU Langone Hospitals - Long Island, Mineola, NY, USA.
José O AlemánHolman Division of Endocrinology, Department of Medicine, NYU Grossman School of Medicine, NY, USA.
Ira J GoldbergDepartment of Pathology and Laboratory Medicine, NYU Grossman Long Island School of Medicine, NYU Langone Hospitals - Long Island, Mineola, NY, USA.
Edward A FisherDepartment of Medicine (Cardiology), The Cardiovascular Research Center, and the Marc and Ruti Bell Program in Vascular Biology, NYU Grossman School of Medicine, NY, NY, USA.
M Mahmood HussainDepartment of Foundations of Medicine, NYU Grossman Long Island School of Medicine, and Diabetes and Obesity Research Center, NYU Langone Hospitals - Long Island, Mineola, NY, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background & Aim: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing health issue. Identifying factors that prevent hepatic lipid accumulation could inform new MASLD prevention or treatment strategies. We previously demonstrated that adipocyte microsomal triglyceride transfer protein (MTP) regulates intracellular lipolysis by inhibiting adipose triglyceride lipase activity. The aim of this study was to investigate the impact of adipose MTP deficiency on MASLD. Methods: We used previously described adipose-specific MTP knockout (A- Results: A- Conclusion: These findings highlight the importance of regulated FA flux from adipose tissue to the liver and the liver's adaptive capacity to utilize adipose-derived FAs in maintaining hepatic health. Modulation of adipocyte FA release may represent a therapeutic strategy to reduce hepatic steatosis. Impact and implications: This study provides significant insights into the role of adipose-specific microsomal triglyceride transfer protein in regulating hepatic lipid metabolism and its potential implications for treating metabolic dysfunction-associated steatotic liver disease. By demonstrating that microsomal triglyceride transfer protein deficiency in adipose tissue leads to increased fatty acid oxidation and reduced hepatic steatosis through enhanced PPARα activation, the research underscores the importance of adipose-liver crosstalk in maintaining liver health. These findings suggest that targeting adipocyte fatty acid release could be a promising therapeutic strategy to mitigate hepatic lipid accumulation and combat metabolic dysfunction-associated steatotic liver disease, offering a novel approach to addressing this growing health issue.

Indexed as

adipose tissueFA oxidationfree fatty acidslipidomiclipoproteinsNAFLDNon-alcoholic fatty liver diseaseperoxisome proliferator-activated receptor alpha

Identifiers

PMID41321937
PMCPMC12657731

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.