Evidence map›Paper›PMID 26805874›Full record

ArticleNutrients2016

Docosahexaenoic Acid Ameliorates Fructose-Induced Hepatic Steatosis Involving ER Stress Response in Primary Mouse Hepatocytes.

Jinying Zheng, Chuan Peng, Yanbiao Ai, Heng Wang, Xiaoqiu Xiao, Jibin Li

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

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  8. Biomedicines · 2020
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  15. FOXA2 alleviates CClScientific reports · 2017
    Article
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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

6 authors at 2 institutions in 1 country.

Jinying ZhengSchool of Public Health and Management, Chongqing Medical University, Research Center for Medicine and Social Development, Innovation Center for Social Risk Governance in Health, Chongqing 400016, China. jinyingzheng1988@163.com.
Chuan PengLaboratory of Lipid & Glucose Metabolism, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China. 13527441813@163.com.
Yanbiao AiSchool of Public Health and Management, Chongqing Medical University, Research Center for Medicine and Social Development, Innovation Center for Social Risk Governance in Health, Chongqing 400016, China. aiyanbiao1992@163.com.
Heng WangLaboratory of Lipid & Glucose Metabolism, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China. hengyy663@163.com.
Xiaoqiu XiaoLaboratory of Lipid & Glucose Metabolism, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China. xiaoxq@cqmu.edu.cn.
Jibin LiSchool of Public Health and Management, Chongqing Medical University, Research Center for Medicine and Social Development, Innovation Center for Social Risk Governance in Health, Chongqing 400016, China. ljb21st@126.com.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The increase in fructose consumption is considered to be a risk factor for developing nonalcoholic fatty liver disease (NAFLD). We investigated the effects of docosahexaenoic acid (DHA) on hepatic lipid metabolism in fructose-treated primary mouse hepatocytes, and the changes of Endoplasmic reticulum (ER) stress pathways in response to DHA treatment. The hepatocytes were treated with fructose, DHA, fructose plus DHA, tunicamycin (TM) or fructose plus 4-phenylbutyric acid (PBA) for 24 h. Intracellular triglyceride (TG) accumulation was assessed by Oil Red O staining. The mRNA expression levels and protein levels related to lipid metabolism and ER stress response were determined by real-time PCR and Western blot. Fructose treatment led to obvious TG accumulation in primary hepatocytes through increasing expression of fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC), two key enzymes in hepatic de novo lipogenesis. DHA ameliorates fructose-induced TG accumulation by upregulating the expression of carnitine palmitoyltransferase 1A (CPT-1α) and acyl-CoA oxidase 1 (ACOX1). DHA treatment or pretreatment with the ER stress inhibitor PBA significantly decreased TG accumulation and reduced the expression of glucose-regulated protein 78 (GRP78), total inositol-requiring kinase 1 (IRE1α) and p-IRE1α. The present results suggest that DHA protects against high fructose-induced hepatocellular lipid accumulation. The current findings also suggest that alleviating the ER stress response seems to play a role in the prevention of fructose-induced hepatic steatosis by DHA.

Indexed as

Stress, PhysiologicalAcetyl-CoA CarboxylaseAnimalsCarnitine O-PalmitoyltransferaseDocosahexaenoic AcidsEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressFatty Acid SynthasesFatty LiverFructoseHeat-Shock ProteinsHepatocytesLipid MetabolismLiverMembrane ProteinsMice4-phenylbutyric acidAcetyl-CoA CarboxylaseCarnitine O-PalmitoyltransferaseDocosahexaenoic AcidsEndoplasmic Reticulum Chaperone BiPErn2 protein, mouseFatty Acid SynthasesFructoseHeat-Shock ProteinsHspa5 protein, mouseMembrane ProteinsPhenylbutyratesProtein Serine-Threonine KinasesTriglyceridesTunicamycindocosahexaenoic acidER stressfructoseNAFLD

Identifiers

PMID26805874
PMCPMC4728666
OpenAlexW2252950443

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.