Evidence map›Paper›PMID 27550859›Full record

ArticleScientific reports2016

Prosteatotic and Protective Components in a Unique Model of Fatty Liver: Gut Microbiota and Suppressed Complement System.

Long Liu, Xing Zhao, Qian Wang, Xiaoxian Sun, Lili Xia, Qianqian Wang, Biao Yang, Yihui Zhang, Sean Montgomery, He Meng and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 76 citations in OpenAlex.

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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

12 authors at 3 institutions in 2 countries.

Long LiuCollege of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Xing ZhaoCollege of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Qian WangCollege of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Xiaoxian SunCollege of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Lili XiaCollege of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Qianqian WangCollege of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Biao YangCollege of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Yihui ZhangCollege of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Sean MontgomeryDepartment of Botany, University of British Columbia, 6270 University Boulevard, British Columbia, V6T 1Z4, Canada.
He MengSchool of Agriculture and Biology, Shanghai Jiaotong University; Shanghai Key Laboratory of Veterinary Biotechnology, 800 Dongchuan Road, Shanghai 200240, China.
Tuoyu GengCollege of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Daoqing GongCollege of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Yangzhou University · CNShanghai Jiao Tong University · CNUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Goose can develop severe hepatic steatosis without overt injury, thus it may serve as a unique model for uncovering how steatosis-related injury is prevented. To identify the markedly prosteatotic and protective mechanisms, we performed an integrated analysis of liver transcriptomes and gut microbial metagenomes using samples collected from overfed and normally-fed geese at different time points. The results indicated that the fatty liver transcriptome, initially featuring a 'metabolism' pathway, was later joined by 'cell growth and death' and 'immune diseases' pathways. Gut microbiota played a synergistic role in the liver response as microbial and hepatic genes affected by overfeeding shared multiple pathways. Remarkably, the complement system, an inflammatory component, was comprehensively suppressed in fatty liver, which was partially due to increased blood lactic acid from enriched Lactobacillus. Data from in vitro studies suggested that lactic acid suppressed TNFα via the HNF1α/C5 pathway. In conclusion, gut microbes and their hosts respond to excess energy influx as an organic whole, severe steatosis and related tolerance of goose liver may be partially attributable to gut microbiotic products and suppressed complement system, and lactic acid from gut microbiota participates in the suppression of hepatic TNFα/inflammation through the HNF1α/C5 pathway.

Indexed as

Gastrointestinal MicrobiomeAnimalsComplement System ProteinsFatty LiverGeeseGene Expression RegulationHepatocyte Nuclear Factor 1-alphaInflammationLactic AcidLactobacillusLiverMetagenomeMicroRNAsTranscriptomeTumor Necrosis Factor-alphaComplement System ProteinsHepatocyte Nuclear Factor 1-alphaLactic AcidMicroRNAsTumor Necrosis Factor-alpha

Identifiers

PMID27550859
PMCPMC4994046
OpenAlexW2515025211

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.