Evidence map›Paper›PMID 32440681›Full record

ArticleBioscience reports2020

ATP reduces mitochondrial MECR protein in liver of diet-induced obese mice in mechanism of insulin resistance.

Shengnan Qian, Li Ma, Shiqiao Peng, Yanhong Xu, Kaiyue Wu, Shuang Shen, Xiaoying Zhang, Yongning Sun, Jianping Ye

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

5 citing papers in PubMed, 13 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

9 authors at 2 institutions in 1 country.

Shengnan QianCollege of Food Science and Technology, College of Fisheries and Life Science, Shanghai Ocean University, Shanghai 201306, China.
Li MaCentral Laboratory, Shanghai Sixth People's Hospital East Campus, Shanghai University of Health and Medical Sciences, Shanghai 201306, China.
Shiqiao PengCentral Laboratory, Shanghai Sixth People's Hospital East Campus, Shanghai University of Health and Medical Sciences, Shanghai 201306, China.
Yanhong XuCentral Laboratory, Shanghai Sixth People's Hospital East Campus, Shanghai University of Health and Medical Sciences, Shanghai 201306, China.
Kaiyue WuCollege of Food Science and Technology, College of Fisheries and Life Science, Shanghai Ocean University, Shanghai 201306, China.
Shuang ShenCentral Laboratory, Shanghai Sixth People's Hospital East Campus, Shanghai University of Health and Medical Sciences, Shanghai 201306, China.
Xiaoying ZhangCentral Laboratory, Shanghai Sixth People's Hospital East Campus, Shanghai University of Health and Medical Sciences, Shanghai 201306, China.
Yongning SunDepartment of Traditional Chinese Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, China.
Jianping YeCentral Laboratory, Shanghai Sixth People's Hospital East Campus, Shanghai University of Health and Medical Sciences, Shanghai 201306, China.
Shanghai University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial 2-enoyl-acyl-carrier protein reductase (MECR) is an enzyme in the mitochondrial fatty acid synthase (mtFAS) pathway. MECR activity remains unknown in the mechanism of insulin resistance in the pathogenesis of type 2 diabetes. In the present study, MECR activity was investigated in diet-induced obese (DIO) mice. Mecr mRNA was induced by insulin in cell culture, and was elevated in the liver of DIO mice in the presence hyperinsulinemia. However, MECR protein was decreased in the liver of DIO mice, and the reduction was blocked by treatment of the DIO mice with berberine (BBR). The mechanism of MECR protein regulation was investigated with a focus on ATP. The protein was decreased in the cell lysate and DIO liver by an increase in ATP levels. The ATP protein reduction was blocked in the liver of BBR-treated mice by suppression of ATP elevation. The MECR protein reduction was associated with insulin resistance and the protein restoration was associated with improvement of insulin sensitivity by BBR in the DIO mice. The data suggest that MECR protein is regulated in hepatocytes by ATP in association with insulin resistance. The study provides evidence for a relationship between MECR protein and insulin resistance.

Indexed as

Diet, High-FatInsulin Resistance3T3-L1 CellsAdenosine TriphosphateAnimalsBerberineDisease Models, AnimalDown-RegulationHepatocytesInsulinLiverMaleMiceMice, Inbred C57BLMitochondria, LiverObesityAdenosine TriphosphateBerberineInsulinOxidoreductases Acting on CH-CH Group Donorstrans-2-enoyl-CoA reductase (NADPH)ATPBerberinehepatic physiologyinsulin resistanceMECRmitochondrial dysfunction

Identifiers

PMID32440681
PMCPMC7273911
OpenAlexW3027471632

What OpenQuestion holds

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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.