Evidence map›Paper›PMID 31894315›Full record

ArticleInternational journal of molecular medicine2020

miR‑146a improves hepatic lipid and glucose metabolism by targeting MED1.

Kun Li, Bao Zhao, Diandian Wei, Wenrui Wang, Yixuan Cui, Lisheng Qian, Guodong Liu

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 3 pooled it
1.4field-weighted citation impact, top 21% 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

36 citing papers in PubMed, 3 syntheses or guidelines pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. The role of impaired mitochondrial function in neurological manifestations of mitochondrial diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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  11. Pancreatic MicroRNAs inBiomolecules · 2025
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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

7 authors at 3 institutions in 1 country.

Kun Li *Department of Biomedical and Health Science, School of Life and Health Science, Anhui Science and Technology University, Fengyang, Anhui 233100, P.R. China.
Bao ZhaoDepartment of Otorhinolaryngology Head and Neck Surgery, First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, P.R. China.
Diandian WeiDepartment of Biomedical and Health Science, School of Life and Health Science, Anhui Science and Technology University, Fengyang, Anhui 233100, P.R. China.
Wenrui WangDepartment of Biotechnology, School of Life Science and Technology, Bengbu Medical College, Bengbu, Anhui 233030, P.R. China.
Yixuan CuiDepartment of Otorhinolaryngology Head and Neck Surgery, First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, P.R. China.
Lisheng QianDepartment of Biomedical and Health Science, School of Life and Health Science, Anhui Science and Technology University, Fengyang, Anhui 233100, P.R. China.
Guodong LiuDepartment of Biomedical and Health Science, School of Life and Health Science, Anhui Science and Technology University, Fengyang, Anhui 233100, P.R. China.
Anhui Science and Technology University · CNFirst Affiliated Hospital of Bengbu Medical College · CNBengbu Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non‑alcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases worldwide. Increasing evidence has shown that microRNAs (miRNAs) play a vital role in the progression of NAFLD. The aim of the present study was to examine the expression level and roles of miR‑146a in fatty liver of high‑fat diet (HFD) and ob/ob mice and fatty acid‑treated hepatic cells using RT‑qPCR and western blot analysis. The results showed that the expression of miR‑146a was significantly decreased in the livers of high‑fat diet (HFD) and ob/ob mice and free fatty acid‑stimulated cells by RT‑qPCR. Overexpression of hepatic miR‑146a improved glucose and insulin tolerance as well as lipid accumulation in the liver by promoting the oxidative metabolism of fatty acids. In addition, the overexpression of miR‑146a increased the amount of mitochondria and promoted mitochondrial respiration in hepatocytes. Similarly, inhibition of miR‑146a expression levels significantly reduced mitochondrial numbers in AML12 cells as well as the expression of mitochondrial respiration related genes. Additionally, MED1 was a direct target of miR‑146a and restoring MED1 abolished the metabolic effects of miR‑146a on lipid metabolism and mitochondrial function. Therefore, results of the present study identified a novel function of miR‑146a in glucose and lipid metabolism in targeting MED1, suggesting that miR‑146a serves as a potential therapeutic target for metabolic syndrome disease.

Indexed as

Lipid MetabolismAnimalsDiet, High-FatDown-RegulationGlucoseLiverMaleMediator Complex Subunit 1Mice, Inbred C57BLMicroRNAsNon-alcoholic Fatty Liver DiseaseUp-RegulationGlucoseMed1 protein, mouseMediator Complex Subunit 1MicroRNAsMirn146 microRNA, mouseMEd1metabolic syndrome diseasemiR-146amitochondrianon-alcoholic fatty liver disease

Identifiers

PMID31894315
PMCPMC6984781
OpenAlexW2997380849

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.