Evidence map›Paper›PMID 34053175›Full record

ArticleJournal of cellular and molecular medicine2021

Metformin protects against insulin resistance induced by high uric acid in cardiomyocytes via AMPK signalling pathways in vitro and in vivo.

Zhenyu Jiao, Yingqun Chen, Yang Xie, Yanbing Li, Zhi Li

Open access · goldFull text read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Exercise pills for cardiometabolic health cannot mimic the exercise milieu.Trends in endocrinology and metabolism: TEM · 2026
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  11. Sexual Dimorphism in Cardiometabolic Diseases: The Role of AMPK.International journal of molecular sciences · 2023
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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

5 authors at 2 institutions in 1 country.

Zhenyu JiaoDepartment of Cardiology, Beijing Chaoyang Hospital, Beijing, China.
Yingqun ChenDepartment of Cardiology, Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China.
Yang XieDepartment of Cardiology, Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China.
Yanbing LiDepartment of Cardiology, Beijing Chaoyang Hospital, Beijing, China.
Zhi LiDepartment of Cardiology, Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China.ORCID 0000-0002-9200-5612
Shantou University · CNBeijing YouAn Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High uric acid (HUA) is associated with insulin resistance (IR) in cardiomyocytes. We investigated whether metformin protects against HUA-induced IR in cardiomyocytes. We exposed primary cardiomyocytes to HUA, and cellular glucose uptake was quantified by measuring the uptake of 2-NBDG, a fluorescent glucose analog. Western blot was used to examine the levels of signalling protein. Membrane of glucose transporter type 4 (GLUT4) was analysed by immunofluorescence. We monitored the impact of metformin on HUA-induced IR and in myocardial tissue of an acute hyperuricaemia mouse model established by potassium oxonate treatment. Treatment with metformin protected against HUA-reduced glucose uptake induced by insulin in cardiomyocytes. HUA directly inhibited the phosphorylation of Akt and the translocation of GLUT4 induced by insulin, which was blocked by metformin. Metformin promoted phosphorylation of AMP-activated protein kinase (AMPK) and restored the insulin-stimulated glucose uptake in HUA-induced IR cardiomyocytes. As a result of these effects, in a mouse model of acute hyperuricaemia, metformin improved insulin tolerance and glucose tolerance, accompanied by increased AMPK phosphorylation, Akt phosphorylation and translocation of GLUT4 in myocardial tissues. As expected, AICAR, another AMPK activator, had similar effects to metformin, demonstrating the important role of AMPK activation in protecting against IR induced by HUA in cardiomyocytes. Metformin protects against IR induced by HUA in cardiomyocytes and improves insulin tolerance and glucose tolerance in an acute hyperuricaemic mouse model, along with the activation of AMPK. Consequently, metformin may be an important potential new treatment strategy for hyperuricaemia-related cardiovascular disease.

Indexed as

Insulin ResistanceAMP-Activated Protein Kinase KinasesAnimalsCells, CulturedGlucoseGlucose Transporter Type 4HyperuricemiaHypoglycemic AgentsMaleMetforminMiceMice, Inbred C57BLMyocytes, CardiacSignal TransductionUric AcidAMP-Activated Protein Kinase KinasesGlucoseGlucose Transporter Type 4Hypoglycemic AgentsMetforminSlc2a4 protein, mouseUric Acidadenosine 5'-monophosphate-activated protein kinasecardiomyocytehigh uric acidinsulin resistancemetformin

Identifiers

PMID34053175
PMCPMC8278091
OpenAlexW3165652890

What Socratic holds

Textfull text, public
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 Socratic graph.