Evidence map›Paper›PMID 31443411›Full record

ArticleNutrients2019

Augmentation of Glucotoxicity, Oxidative Stress, Apoptosis and Mitochondrial Dysfunction in HepG2 Cells by Palmitic Acid.

Arwa Alnahdi, Annie John, Haider Raza

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

66 citing papers in PubMed, 128 citations in OpenAlex.

  1. Review
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6 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

3 authors at 1 institution in 1 country.

Arwa AlnahdiDepartment of Biochemistry, College of Medicine and Health Sciences, UAE University, P.O. Box-17666, Al Ain, UAE.
Annie JohnDepartment of Biochemistry, College of Medicine and Health Sciences, UAE University, P.O. Box-17666, Al Ain, UAE.
Haider RazaDepartment of Biochemistry, College of Medicine and Health Sciences, UAE University, P.O. Box-17666, Al Ain, UAE. H.Raza@uaeu.ac.ae.
United Arab Emirates University · AE

Funding

Sheikh Hamdan Bin Rashid Al Maktoum Award for Medical Sciences MRG-18/2013-2014
6 · The paper itself

Abstract

Hyperglycemia and hyperlipidemia are the hallmarks of diabetes and obesity. Experimental and epidemiological studies have suggested that dietary management and caloric restriction are beneficial in reducing the complications of diabesity. Studies have suggested that increased availability of energy metabolites like glucose and saturated fatty acids induces metabolic, oxidative, and mitochondrial stress, accompanied by inflammation that may lead to chronic complications in diabetes. In the present study, we used human hepatoma HepG2 cells to investigate the effects of high glucose (25 mM) and high palmitic acid (up to 0.3 mM) on metabolic-, inflammatory-, and redox-stress-associated alterations in these cells. Our results showed increased lipid, protein, and DNA damage, leading to caspase-dependent apoptosis and mitochondrial dysfunction. Glucolipotoxicity increased ROS production and redox stress appeared to alter mitochondrial membrane potential and bioenergetics. Our results also demonstrate the enhanced ability of cytochrome P450s-dependent drug metabolism and antioxidant adaptation in HepG2 cells treated with palmitic acid, which was further augmented with high glucose. Altered NF-kB/AMPK/mTOR-dependent cell signaling and inflammatory (IL6/TNF-α) responses were also observed. Our results suggest that the presence of high-energy metabolites enhances apoptosis while suppressing autophagy by inducing inflammatory and oxidative stress responses that may be responsible for alterations in cell signaling and metabolism.

Indexed as

AMP-Activated Protein KinasesApoptosisAutophagyEnergy MetabolismGlucoseHepatocytesHep G2 CellsHumansInflammation MediatorsMitochondria, LiverNF-kappa BOxidative StressPalmitic AcidSignal TransductionTOR Serine-Threonine KinasesAMP-Activated Protein KinasesGlucoseInflammation MediatorsMTOR protein, humanNF-kappa BPalmitic AcidTOR Serine-Threonine KinasesapoptosisglucolipotoxicityHepG2 cellsmitochondrial dysfunctionpalmitic acidredox metabolism

Identifiers

PMID31443411
PMCPMC6770774
OpenAlexW2969456983

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.