Evidence map›Paper›PMID 31173239›Full record

ArticleMolecular medicine reports2019

MicroRNA‑802 increases hepatic oxidative stress and induces insulin resistance in high‑fat fed mice.

Xi Yang, Hanying Xing, Jingzhen Liu, Linquan Yang, Huan Ma, Huijuan Ma

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. 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
0.9field-weighted citation impact, top 31% 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, 19 citations in OpenAlex.

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  14. The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress.International journal of molecular sciences · 2020
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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 1 institution in 1 country.

Xi YangDepartment of Endocrinology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.
Hanying XingHebei Key Laboratory of Metabolic Disease, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.
Jingzhen LiuDepartment of Endocrinology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.
Linquan YangHebei Key Laboratory of Metabolic Disease, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.
Huan MaHebei Key Laboratory of Metabolic Disease, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.
Huijuan MaDepartment of Endocrinology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.
Hebei General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The expression of microRNA‑802 (miR‑802) is known to be associated with insulin resistance (IR); however, the mechanism remains unclear. The present study investigated how miR‑802 contributes to the development of IR using C57BL/6J mice fed a high‑fat diet (HFD) to establish a model of IR. Adeno‑associated virus overexpressing miR‑802 was administered to the mice via tail vein injection. The effects of miR‑802 on reactive oxygen species (ROS), lipid peroxidation (LPO) and the activities of multiple ROS‑related enzymes were investigated. Western blot analysis was used to estimate the protein levels of extracellular signal regulated kinase (ERK), p38mitogen‑activated protein kinases (p38MAPK), c‑Jun N‑terminal kinase (JNK), insulin receptor substrate 1 (IRS‑1) and protein kinase B (AKT1). The results demonstrated that the levels of ROS and LPO production were increased in the livers of the miR‑802‑treated group compared with the control group. The activities of the ROS‑related enzymes were reduced. Furthermore, the expression of phosphorylated (phosphor)‑p38MAPK and phosphor‑JNK were upregulated in the miR‑802 overexpression group, whereas there was no difference in the expression levels of phosphor‑ERK. The expression levels of phosphor‑AKT1 were reduced in the miR‑802‑treated group and these effects were reversed by miR‑802 knockdown. In conclusion, the results demonstrate that miR‑802 may cause IR by activating the JNK and p38MAPK pathways to increase hepatic oxidative stress.

Indexed as

Diet, High-FatFeeding BehaviorAnimalsAntioxidantsBiomarkersBody WeightGene Expression RegulationGlucose IntoleranceInsulinInsulin ResistanceLiverMaleMAP Kinase Signaling SystemMice, Inbred C57BLMicroRNAsOxidative StressAntioxidantsBiomarkersInsulinMicroRNAsMIRN802 microRNA, mouseReactive Oxygen Species

Identifiers

PMID31173239
PMCPMC6625421
OpenAlexW2948992027

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.