Evidence map›Paper›PMID 31392349›Full record

ArticleCellular and molecular life sciences : CMLS2020

Lipophagy mediated carbohydrate-induced changes of lipid metabolism via oxidative stress, endoplasmic reticulum (ER) stress and ChREBP/PPARγ pathways.

Tao Zhao, Kun Wu, Christer Hogstrand, Yi-Huan Xu, Guang-Hui Chen, Chuan-Chuan Wei, Zhi Luo

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
10.4field-weighted citation impact, top 1% 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

63 citing papers in PubMed, 167 citations in OpenAlex.

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  13. Roles of X-box binding protein 1 in liver pathogenesis.Clinical and molecular hepatology · 2025
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3 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

7 authors at 2 institutions in 2 countries.

Tao ZhaoKey Laboratory of Freshwater Animal Breeding, Ministry of Agriculture, Fishery College, Huazhong Agricultural University, Wuhan, 430070, China.
Kun WuKey Laboratory of Freshwater Animal Breeding, Ministry of Agriculture, Fishery College, Huazhong Agricultural University, Wuhan, 430070, China.
Christer HogstrandDiabetes and Nutritional Sciences Division, School of Medicine, King's College London, London, UK.
Yi-Huan XuKey Laboratory of Freshwater Animal Breeding, Ministry of Agriculture, Fishery College, Huazhong Agricultural University, Wuhan, 430070, China.
Guang-Hui ChenKey Laboratory of Freshwater Animal Breeding, Ministry of Agriculture, Fishery College, Huazhong Agricultural University, Wuhan, 430070, China.
Chuan-Chuan WeiKey Laboratory of Freshwater Animal Breeding, Ministry of Agriculture, Fishery College, Huazhong Agricultural University, Wuhan, 430070, China.
Zhi LuoKey Laboratory of Freshwater Animal Breeding, Ministry of Agriculture, Fishery College, Huazhong Agricultural University, Wuhan, 430070, China. luozhi99@mail.hzau.edu.cn.ORCID http://orcid.org/0000-0003-3219-1609
Huazhong Agricultural University · CNKing's College London · GB

Funding

Fundamental Research Funds for the Central Universities, China 2662018PY089National Key R&D Program of China 2018YFD0900400
6 · The paper itself

Abstract

High-carbohydrate diets (HCD) can induce the occurrence of nonalcoholic fatty liver disease (NAFLD), characterized by dramatic accumulation of hepatic lipid droplets (LDs). However, the potential molecular mechanisms are still largely unknown. In this study, we investigated the role of autophagy in the process of HCD-induced changes of hepatic lipid metabolism, and to examine the process of underlying mechanisms during these molecular contexts. We found that HCD significantly increased hepatic lipid accumulation and activated autophagy. Using primary hepatocytes, we found that HG increased lipid accumulation and stimulated the release of NEFA by autophagy-mediated lipophagy, and that lipophagy significantly alleviated high glucose (HG)-induced lipid accumulation. Oxidative and endoplasmic reticulum (ER) stress pathways played crucial regulatory roles in HG-induced lipophagy activation and HG-induced changes of lipid metabolism. Further investigation found that HG-activated lipophagy and HG-induced changes of lipid metabolism were via enhancing carbohydrate response element-binding protein (ChREBP) DNA binding capacity at PPARγ promoter region, which in turn induced transcriptional activation of the key genes related to lipogenesis and autophagy. The present study, for the first time, revealed the novel mechanism for lipophagy mediating HCD-induced changes of lipid metabolism by oxidative stress and ER stress, and ChREBP/PPARγ pathways. Our study provided innovative evidence for the direct relationship between carbohydrate and lipid metabolism via ChREBP/PPARγ pathway.

Indexed as

AnimalsAutophagyBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCarbohydratesCatfishesDisease Models, AnimalDNA-Binding ProteinsEndoplasmic Reticulum StressGlucoseHepatocytesHumansLipid DropletsLipid MetabolismLipogenesisLiverNon-alcoholic Fatty Liver DiseaseBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCarbohydratesDNA-Binding ProteinsGlucosePPAR gammaDietary carbohydrateLipid depositionLipid metabolismLipophagyRegulatory pathways

Identifiers

PMID31392349
PMCPMC11105093
OpenAlexW2965405792

What OpenQuestion holds

Textmetadata
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.