Evidence map›Paper›PMID 34870551›Full record

ArticlePharmaceutical biology2022

Ellagic acid protects against non-alcoholic fatty liver disease in streptozotocin-diabetic rats by activating AMPK.

Jozaa Z ALTamimi, Ghedeir M Alshammari, Nora A AlFaris, Reham I Alagal, Dalal H Aljabryn, Norah A Albekairi, Mahmoud Ahmad Alkhateeb, Mohammed Abdo Yahya

Open access · goldAbstract read
In one paragraph

Article in Pharmaceutical biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.1field-weighted citation impact, top 3% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

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  9. Regulation mechanism ofFrontiers in nutrition · 2025
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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.

Jozaa Z ALTamimiNutrition and Food Science, Department of Physical Sport Science, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia.ORCID 0000-0002-5510-0768
Ghedeir M AlshammariDepartment of Food Science and Nutrition, College of Food and Agricultural Sciences, King Saud University, Riyadh, Saudi Arabia.ORCID 0000-0002-2043-1209
Nora A AlFarisNutrition and Food Science, Department of Physical Sport Science, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia.ORCID 0000-0002-9135-5725
Reham I AlagalNutrition and Food Science, Department of Physical Sport Science, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia.ORCID 0000-0002-8515-1574
Dalal H AljabrynNutrition and Food Science, Department of Physical Sport Science, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia.ORCID 0000-0002-4125-1303
Norah A AlbekairiDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
Mahmoud Ahmad AlkhateebDepartment of Basic Medical Sciences, College of Medicine, King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), Riyadh, Saudi Arabia.
Mohammed Abdo YahyaDepartment of Food Science and Nutrition, College of Food and Agricultural Sciences, King Saud University, Riyadh, Saudi Arabia.ORCID 0000-0002-5665-9600
Princess Nourah bint Abdulrahman University · SAKing Saud University · SAKing Saud bin Abdulaziz University for Health Sciences · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextEllagic acid (EA) is used in traditional medicine to treated hyperlipidaemia.

objectiveThis study examined if AMPK mediates the anti-steatotic effect of ellagic acid (EA) in streptozotocin (STZ)-induced type 1 diabetes mellitus in rats. MATERIALS AND

methodsAdult male Wistar rats (130 ± 10 g) were divided into 6 groups (

resultsIn T1DM-rats, EA reduced fasting glucose levels (44.8%), increased fasting insulin levels (92.8%), prevented hepatic lipid accumulation, and decreased hepatic and serum levels of total triglycerides (54% & 61%), cholesterol (57% & 48%), and free fatty acids (40% & 37%). It also reduced hepatic levels of ROS (62%), MDA (52%), TNF-α (62%), and IL-6 (57.2%) and the nuclear activity of NF-κB p65 (54%) but increased the nuclear activity of Nrf-2 (4-fold) and levels of GSH (107%) and SOD (87%). Besides, EA reduced downregulated SREBP1 (35%), SREBP2 (34%), ACC-1 (36%), FAS (38%), and HMG-CoAR (49%) but stimulated mRNA levels of PPARα (1.7-fold) and CPT1a (1.8-fold), CPT1b (2.9-fold), and p-AMPK (4-fold). All these events were prevented by the co-administration of CC. DISCUSSION AND

conclusionsThese findings encourage the use of EA to treat hepatic disorders, and non-alcoholic fatty liver disease (NAFLD). Further

Indexed as

AMP-Activated Protein KinasesAnimalsBlood GlucoseDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Ellagic AcidInsulinMaleNon-alcoholic Fatty Liver DiseaseRatsRats, WistarStreptozocinAMP-Activated Protein KinasesBlood GlucoseEllagic AcidInsulinStreptozocininflammationlipid metabolismNAFLDoxidative stresspolyphenolsT1DM

Identifiers

PMID34870551
PMCPMC8654409
OpenAlexW4200076301

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.