Evidence map›Paper›PMID 35452750›Full record

ArticleAlcohol (Fayetteville, N.Y.)2022

Elevated stearoyl-CoA desaturase 1 activity is associated with alcohol-associated liver disease.

T D Klepp, M E Sloan, Soundarya Soundararajan, C E Ramsden, R Cinar, M L Schwandt, N Diazgranados, V Vatsalya, V A Ramchandani

Open access · greenAbstract read
In one paragraph

Article in Alcohol (Fayetteville, N.Y.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Lipid Droplet Dynamics in Alcoholic Steatohepatitis.The American journal of pathology · 2026
    Review
  5. Loss ofZoological research · 2024
    Article
  6. Article
  7. 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

9 authors at 2 institutions in 2 countries.

T D KleppOffice of the Clinical Director, National Institute on Alcohol Abuse and Alcoholism (NIAAA), National Institutes of Health (NIH), Bethesda, MD, United States.
M E SloanHuman Psychopharmacology Laboratory, NIAAA, NIH, Bethesda, MD, United States; Addictions Division, Centre for Addiction and Mental Health, Toronto, Ontario, Canada; Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, Ontario, Canada; Division of Neurosciences and Clinical Translation, Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada; Department of Pharmacology & Toxicology, University of Toronto, Toronto, Ontario, Canada; Department of Psychological Clinical Science, University of Toronto, Toronto, Ontario, Canada.
Soundarya SoundararajanHuman Psychopharmacology Laboratory, NIAAA, NIH, Bethesda, MD, United States.
C E RamsdenLipid Mediators, Inflammation and Pain Unit, Laboratory of Clinical Investigation, National Institute on Aging, Baltimore, MD, United States; Division of Intramural Clinical and Biological Research, NIAAA, NIH, Bethesda, MD, United States.
R CinarSection on Fibrotic Disorders, NIAAA, NIH, Bethesda, MD, United States.
M L SchwandtOffice of the Clinical Director, National Institute on Alcohol Abuse and Alcoholism (NIAAA), National Institutes of Health (NIH), Bethesda, MD, United States.
N DiazgranadosOffice of the Clinical Director, National Institute on Alcohol Abuse and Alcoholism (NIAAA), National Institutes of Health (NIH), Bethesda, MD, United States.
V VatsalyaHuman Psychopharmacology Laboratory, NIAAA, NIH, Bethesda, MD, United States; Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, and Alcohol Research Center, University of Louisville School of Medicine, Louisville, KY, United States; Robley Rex Veterans Administration Medical Center, Louisville, KY, United States. Electronic address: v0vats01@louisville.edu.
V A RamchandaniHuman Psychopharmacology Laboratory, NIAAA, NIH, Bethesda, MD, United States. Electronic address: vijayr@mail.nih.gov.
National Institutes of Health · USNational Institute on Alcohol Abuse and Alcoholism · US

Funding

NIAAA Repository/Screening Database Management and ResearchZIAAA000130 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI SCHWANDT, MELANIE · 2017 to 2025
$60.1M
The roles of lipid mediators in inflammation, pain, and neuro-degenerationZIAAG000453 · NIA · NATIONAL INSTITUTE ON AGING · PI RAMSDEN, CHRISTOPHER · 2017 to 2025
$35.1M
Alcohol Pharmacokinetics and Pharmacodynamics in HumansZIAAA000466 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI RAMCHANDANI, VIJAY ARJUN · 2009 to 2025
$31.2M
Alcohol Pharmacokinetics and Pharmacodynamics in HumansZ01AA000466 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI RAMCHANDANI, VIJAY ARJUN · 2006 to 2008
$762k
Lactobacillus rhamnosus: A Novel Probiotic Therapy for treating Alcohol Use DisorderK23AA029198 · NIAAA · UNIVERSITY OF LOUISVILLE · PI VATSALYA, VATSALYA · 2021 to 2025
$704k
Intramural NIH HHS Z01 AA000466NIAAA NIH HHS K23 AA029198
6 · The paper itself

Abstract

Chronic binge drinking induces hepatic lipid accumulation, but only certain individuals develop alcohol-associated liver disease (ALD). Specific patterns of lipid accumulation are thought to be associated with ALD, but this has not been comprehensively investigated to date. We analyzed plasma fatty acid levels, quantified by gas chromatography-mass spectrometry, in a sample of patients with alcohol use disorder (AUD). Given that elevation in serum alanine transaminase (ALT) levels are strongly associated with ALD, patients were stratified into two groups based on ALT levels: an ALD group (ALT >40 IU/L) and a non-ALD group (ALT ≤40 IU/L). There was a shift toward greater concentrations of monounsaturated fatty acids in the ALD group compared to the non-ALD group. Stearoyl-CoA desaturase (SCD1) activity in the ALD group was then estimated as the ratio of palmitoleic acid (16:1) to palmitic acid (16:0). SCD1 activity was greater in the ALD than the non-ALD group. A series of linear regression models demonstrated that SCD1 activity mediated the association between binge drinking and ALD. These findings provide initial evidence that SCD1 activity may be associated with ALD. If validated prospectively, elevated SCD1 activity could potentially be used as a biomarker to identify individuals at high risk for developing ALD.

Indexed as

Binge DrinkingFatty LiverLiver Diseases, AlcoholicStearoyl-CoA DesaturaseFatty AcidsHumansLiverFatty AcidsSCD1 protein, humanStearoyl-CoA Desaturasealcohol-associated liver diseasealcohol use disorderbinge drinkingfatty acidspalmitoleic acidstearoyl-CoA desaturase

Identifiers

PMID35452750
PMCPMC9256783
OpenAlexW4224278555

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.