Article in American journal of physiology. Gastrointestinal and liver physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
0numbers the graph read from it
0cells of the map it votes in
3citing 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.
Mukund SrinivasanDepartment of Pathology, The University of Texas Medical Branch, Galveston, Texas, United States.ORCID 0000-0002-3307-2305
Sumedha KotaDepartment of Pathology, The University of Texas Medical Branch, Galveston, Texas, United States.
Kamlesh BhopaleDepartment of Pathology, The University of Texas Medical Branch, Galveston, Texas, United States.
Anna CaracheoDepartment of Pathology, The University of Texas Medical Branch, Galveston, Texas, United States.
Lata KaphaliaDepartment of Internal Medicine, The University of Texas Medical Branch, Galveston, Texas, United States.
Jennifer LinaresMass Spectrometry Facility, Department of Biochemistry and Molecular Biology, The University of Texas Medical Branch, Galveston, Texas, United States.
Trevor RomsdahlMass Spectrometry Facility, Department of Biochemistry and Molecular Biology, The University of Texas Medical Branch, Galveston, Texas, United States.ORCID 0000-0001-9075-9771
William RussellMass Spectrometry Facility, Department of Biochemistry and Molecular Biology, The University of Texas Medical Branch, Galveston, Texas, United States.ORCID 0000-0003-1931-4555
Vsevolod PopovDepartment of Pathology, The University of Texas Medical Branch, Galveston, Texas, United States.
Paul BoorDepartment of Pathology, The University of Texas Medical Branch, Galveston, Texas, United States.
Bhupendra KaphaliaDepartment of Pathology, The University of Texas Medical Branch, Galveston, Texas, United States.ORCID 0000-0002-3794-0392
Funding
Role of Alcohol Metabolism in Alcoholic Chronic PancreatitisR01AA025850 · NIAAA · UNIVERSITY OF TEXAS MED BR GALVESTON · PI KAPHALIA, BHUPENDRA S · 2017 to 2021
$1.7M
AMPKa agonist in attenuating CPT1A inhibition and alcoholic chronic pancreatitisR21AA030883 · NIAAA · UNIVERSITY OF TEXAS MED BR GALVESTON · PI KAPHALIA, BHUPENDRA S · 2023 to 2023
$420k
AMPK Signaling and Chronic Alcoholic PancreatitisR21AA024699 · NIAAA · UNIVERSITY OF TEXAS MED BR GALVESTON · PI KAPHALIA, BHUPENDRA S · 2016 to 2017
$407k
Cancer Prevention and Research Institute of Texas (CPRIT) RP190682HHS | NIH | National Institute on Alcohol Abuse and Alcoholism (NIAAA) AA030883HHS | NIH | National Institute on Alcohol Abuse and Alcoholism (NIAAA) AA24699HHS | NIH | National Institute on Alcohol Abuse and Alcoholism (NIAAA) AA25850NIAAA NIH HHS R01 AA025850NIAAA NIH HHS R21 AA024699NIAAA NIH HHS R21 AA030883
6 · The paper itself
Abstract
Alcohol use disorder is a major risk factor for alcohol-associated liver disease (ALD), characterized by reduced hepatic alcohol dehydrogenase (ADH) activity, increased body burden of alcohol, and its nonoxidative metabolism to fatty acid ethyl esters (FAEEs). However, the mechanism(s) underlying ALD remain unclear. This study investigated the metabolic basis and mechanism(s) of ALD in chronic ethanol (EtOH)-fed hepatic ADH1-deficient (ADH
Indexed as
Alcohol DehydrogenaseEthanolLiverLiver Diseases, AlcoholicAMP-Activated Protein KinasesAnimalsDisease Models, AnimalMaleMiceOxidative StressAlcohol DehydrogenaseAMP-Activated Protein KinasesEthanolAlcohol-associated liver diseasealcohol dehydrogenaseAMPKα signalingdeer micefatty acid ethyl esters
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.
Dysregulated hepatic alcohol metabolism: a key factor involved in the pathogenesis of alcohol-associated liver disease. · full record | OpenQuestion