Evidence map›Paper›PMID 32970287›Full record

ArticleEndocrine2020

Metformin downregulates miR223 expression in insulin-resistant 3T3L1 cells and human diabetic adipose tissue.

Yousof Naghiaee, Reza Didehdar, Fatemeh Pourrajab, Masoud Rahmanian, Naeime Heiranizadeh, Azra Mohiti, Javad Mohiti-Ardakani

Abstract read
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In one paragraph

Article in Endocrine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 28% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Adipose Tissue Dysfunction in Polycystic Ovary Syndrome.The Journal of clinical endocrinology and metabolism · 2023
    Pooled it
  2. Review
  3. Review
  4. Molecular Mechanism of Metformin Regulating the Regeneration of PlanarianInternational journal of molecular sciences · 2025
    Article
  5. Review
  6. Review
  7. Article
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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 1 institution in 1 country.

Yousof NaghiaeeDepartment of Biochemistry and Molecular Biology, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Reza DidehdarDepartment of Biochemistry, Faculty of Medicine, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Fatemeh PourrajabDepartment of Biochemistry and Molecular Biology, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Masoud RahmanianDepartment of Endocrinology, School of Medicine Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Naeime HeiranizadehDepartment of General Surgery, School of Medicine Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Azra MohitiDepartment of Oral Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Javad Mohiti-ArdakaniDepartment of Biochemistry and Molecular Biology, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. mohiti@ssu.ac.ir.
Shahid Sadoughi University of Medical Sciences and Health Services · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims and designsMetformin, an anti-diabetic drug, is the first line medication for the treatment of type 2 diabetes mellitus and some studies show its relationship with micro-RNAs. This study set up to determine the effect of metformin on miR223 expression and content of AKT/GLUT4 proteins in insulin resistant signaling in 3T3L1 cells and adipocyte of human diabetic patients. MATERIALS AND

methodsSubcutaneous adipose tissues were taken from newly diagnosed diabetic patients (HOMA-IR > 1.8), before and after three months treatment with 500 mg of metformin twice a day. Cellular homogenate was prepared and miR223 expression and AKT/GLUT4 protein expression were determined by quantitative real-time PCR and western blotting. The results were compared to insulin resistant 3T3L1 adipocytes that were treated with 10 mM Metformin.

resultsMiR223 expression was significantly overexpressed both in insulin-resistant 3T3L1 adipocytes compared to non-insulin resistant adipocytes and in human diabetic adipose tissue, compared to non-diabetics (P value < 0.01). Metformin treatment downregulated miR223 expression in both adipocytes and human diabetic adipose tissue. In contrast the IRS/PI3-K/AKT pathway signaling components, Akt and GLUT4 increased in insulin-resistant 3T3L1 adipocytes and human diabetic adipose tissue after three months of metformin treatment.

conclusionsMetformin reduced insulin resistance in adipocytes by reduction of miR223 expression and improving of IRS/Akt/GLUT4 signaling pathways. Plasma miR223 expression of human diabetic patients was reduced by metformin treatment. These results point to a novel mechanism of miR223 in insulin resistance.

Indexed as

Diabetes Mellitus, Type 2Insulin ResistanceMetforminMicroRNAs3T3-L1 CellsAdipocytesAdipose TissueAnimalsGlucose Transporter Type 4HumansInsulinMiceGlucose Transporter Type 4InsulinMetforminMicroRNAsMIR223, humanMIRN223 microRNA, mouse3T3L1adipocytesInsulin resistanceMetforminmiR223type 2 diabetes mellitus

Identifiers

PMID32970287
OpenAlexW3088471284

What Socratic holds

Texttitle and abstract
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.