Evidence map›Paper›PMID 31484323›Full record

ArticleNutrients2019

Indole-3-Acetic Acid Alleviates Nonalcoholic Fatty Liver Disease in Mice via Attenuation of Hepatic Lipogenesis, and Oxidative and Inflammatory Stress.

Yun Ji, Yuan Gao, Hong Chen, Yue Yin, Weizhen Zhang

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 155 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
155citing papers in PubMed, 1 pooled it
15.0field-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

155 citing papers in PubMed, 1 synthesis or guideline pooled it, 271 citations in OpenAlex.

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95 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

5 authors at 1 institution in 1 country.

Yun JiDepartment of Physiology and Pathophysiology, Peking University Health Science Center, Beijing 100191, China.ORCID 0000-0002-3483-0729
Yuan GaoDepartment of Physiology and Pathophysiology, Peking University Health Science Center, Beijing 100191, China.
Hong ChenDepartment of Physiology and Pathophysiology, Peking University Health Science Center, Beijing 100191, China.
Yue YinDepartment of Physiology and Pathophysiology, Peking University Health Science Center, Beijing 100191, China.
Weizhen ZhangDepartment of Physiology and Pathophysiology, Peking University Health Science Center, Beijing 100191, China. weizhenzhang@bjmu.edu.cn.ORCID 0000-0001-8791-2798
Peking University · CN

Funding

the National Key R&D Program of China 2017YFC0908900the National Natural Science Foundation of China 81730020the Projects funded by China Postdoctoral Science Foundation 2018M641113
6 · The paper itself

Abstract

Recent evidences have linked indole-3-acetic acid (IAA), a gut microbiota-derived metabolite from dietary tryptophan, with the resistance to liver diseases. However, data supporting IAA-mediated protection against nonalcoholic fatty liver disease (NAFLD) from an in vivo study is lacking. In this study, we assessed the role of IAA in attenuating high-fat diet (HFD)-induced NAFLD in male C57BL/6 mice. Administration of IAA (50 mg/kg body weight) by intraperitoneal injection was found to alleviate HFD-induced elevation in fasting blood glucose and homeostasis model assessment of insulin resistance (HOMA-IR) index as well as plasma total cholesterol, low-density lipoprotein cholesterol (LDL-C), and glutamic-pyruvic transaminase (GPT) activity. Histological examination further presented the protective effect of IAA on liver damage induced by HFD feeding. HFD-induced an increase in liver total triglycerides and cholesterol, together with the upregulation of genes related to lipogenesis including sterol regulatory element binding-protein 1 (Srebf1), steraroyl coenzyme decarboxylase 1 (Scd1), peroxisome proliferator-activated receptor gamma (PPARγ), acetyl-CoA carboxylase 1 (Acaca), and glycerol-3-phosphate acyltransferase, mitochondrial (Gpam), which were mitigated by IAA treatment. The results of reactive oxygen species (ROS) and malonaldehyde (MDA) level along with superoxide dismutase (SOD) activity and glutathione (GSH) content in liver tissue evidenced the protection of IAA against HFD-induced oxidative stress. Additionally, IAA attenuated the inflammatory response of liver in mice exposed to HFD as shown by the reduction in the F4/80-positive macrophage infiltration and the expression of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-α (TNF-α). In conclusion, our findings uncover that IAA alleviates HFD-induced hepatotoxicity in mice, which proves to be associated with the amelioration in insulin resistance, lipid metabolism, and oxidative and inflammatory stress.

Indexed as

AnimalsIndoleacetic AcidsInflammationLipidsLipogenesisLiverMaleMiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseOxidative Stressindoleacetic acidIndoleacetic AcidsLipidsindole-3-acetic acidinflammationlipid metabolismNAFLDoxidative stresssteatosis

Identifiers

PMID31484323
PMCPMC6769627
OpenAlexW2972269795

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.