Evidence map›Paper›PMID 32782332›Full record

ArticleScientific reports2020

Metformin reduces saturated fatty acid-induced lipid accumulation and inflammatory response by restoration of autophagic flux in endothelial cells.

Hae-Suk Kim, Guang Ren, Teayoun Kim, Sushant Bhatnagar, Qinglin Yang, Young Yil Bahk, Jeong-A Kim

Open access · goldFull text read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 68 citations in OpenAlex.

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  11. Severe Insulin Resistance Syndromes: Clinical Spectrum and Management.International journal of molecular sciences · 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 2 institutions in 2 countries.

Hae-Suk KimDepartment of Medicine, Division of Endocrinology, Diabetes, and Metabolism, Comprehensive Diabetes Center, University of Alabama at Birmingham, 1825 University Blvd, Birmingham, AL, 35294, USA.
Guang RenDepartment of Medicine, Division of Endocrinology, Diabetes, and Metabolism, Comprehensive Diabetes Center, University of Alabama at Birmingham, 1825 University Blvd, Birmingham, AL, 35294, USA.
Teayoun KimDepartment of Medicine, Division of Endocrinology, Diabetes, and Metabolism, Comprehensive Diabetes Center, University of Alabama at Birmingham, 1825 University Blvd, Birmingham, AL, 35294, USA.
Sushant BhatnagarDepartment of Medicine, Division of Endocrinology, Diabetes, and Metabolism, Comprehensive Diabetes Center, University of Alabama at Birmingham, 1825 University Blvd, Birmingham, AL, 35294, USA.
Qinglin YangDepartment of Nutrition, University of Alabama at Birmingham, Birmingham, AL, USA.
Young Yil BahkDepartment of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju, 27478, Republic of Korea.
Jeong-A KimDepartment of Medicine, Division of Endocrinology, Diabetes, and Metabolism, Comprehensive Diabetes Center, University of Alabama at Birmingham, 1825 University Blvd, Birmingham, AL, 35294, USA. jakim@uab.edu.
University of Alabama at Birmingham · USKonkuk University · KR

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
Saturated Fatty Acid-induced Autophagy in Vascular EndotheliumR01HL128695 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KIM, JEONGA · 2016 to 2019
$1.8M
Anti-obesity effect of NO-releasing NanomatrixR03AG058078 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KIM, JEONGA · 2018 to 2019
$149k
NHLBI NIH HHS R01 HL128695NIA NIH HHS R03 AG058078NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

Autophagy, an integral part of the waste recycling process, plays an important role in cellular physiology and pathophysiology. Impaired autophagic flux causes ectopic lipid deposition, which is defined as the accumulation of lipids in non-adipose tissue. Ectopic lipid accumulation is observed in patients with cardiometabolic syndrome, including obesity, diabetes, insulin resistance, and cardiovascular complications. Metformin is the first line of treatment for type 2 diabetes, and one of the underlying mechanisms for the anti-diabetic effect of metformin is mediated by the stimulation of AMP-activated protein kinase (AMPK). Because the activation of AMPK is crucial for the initiation of autophagy, we hypothesize that metformin reduces the accumulation of lipid droplets by increasing autophagic flux in vascular endothelial cells. Incubation of vascular endothelial cells with saturated fatty acid (SFA) increased the accumulation of lipid droplets and impaired autophagic flux. We observed that the accumulation of lipid droplets was reduced, and the autophagic flux was enhanced by treatment with metformin. The knock-down of AMPKα by using siRNA blunted the effect of metformin. Furthermore, treatment with SFA or inhibition of autophagy increased leukocyte adhesion, whereas treatment with metformin decreased the SFA-induced leukocyte adhesion. The results suggest a novel mechanism by which metformin protects vascular endothelium from SFA-induced ectopic lipid accumulation and pro-inflammatory responses. In conclusion, improving autophagic flux may be a therapeutic strategy to protect endothelial function from dyslipidemia and diabetic complications.

Indexed as

AutophagyAMP-Activated Protein KinasesAnimalsCarnitine O-PalmitoyltransferaseEndothelium, VascularFatty AcidsHypoglycemic AgentsInflammationInsulin ResistanceLipid MetabolismMetforminMiceMice, Inbred C57BLMice, KnockoutAMP-Activated Protein KinasesCarnitine O-PalmitoyltransferaseCPT1B protein, mouseFatty AcidsHypoglycemic AgentsMetformin

Identifiers

PMID32782332
PMCPMC7419289
OpenAlexW3048788378

What OpenQuestion 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 OpenQuestion graph.