Evidence map›Paper›PMID 31139382›Full record

ArticleFood science & nutrition2019

Metformin-induced autophagy and irisin improves INS-1 cell function and survival in high-glucose environment via AMPK/SIRT1/PGC-1α signal pathway.

Qingxue Li, Shaohui Jia, Lei Xu, Biao Li, Ning Chen

Open access · hybridAbstract read
In one paragraph

Article in Food science & nutrition, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 76 citations in OpenAlex.

  1. SIRT1 in Neurodegenerative Diseases: Molecular Mechanisms, Disease Relevance, and Therapeutic Potential.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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.

Qingxue LiTianjiu Research and Development Center for Exercise Nutrition and Foods, Hubei Key Laboratory of Sport Training and Monitoring, College of Health Science Wuhan Sports University Wuhan China.
Shaohui JiaTianjiu Research and Development Center for Exercise Nutrition and Foods, Hubei Key Laboratory of Sport Training and Monitoring, College of Health Science Wuhan Sports University Wuhan China.
Lei XuGraduate School Wuhan Sports University Wuhan China.
Biao LiGraduate School Wuhan Sports University Wuhan China.
Ning ChenTianjiu Research and Development Center for Exercise Nutrition and Foods, Hubei Key Laboratory of Sport Training and Monitoring, College of Health Science Wuhan Sports University Wuhan China.ORCID https://orcid.org/0000-0002-8191-6744
Wuhan Sports University · CNLinyi University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In order to explore the protective function of metformin on pancreatic β cells to alleviate insulin resistance and underlying mechanisms, INS-1 cells were cultured into normal control (N), high glucose (H), high glucose and metformin (H + Met), high glucose and chloroquine (H + CQ), and high glucose and Ex527 (H + Ex527) groups, respectively. Upon 24-hr cultivation, the proliferation and glucose-stimulated insulin secretion (GSIS) of INS-1 cells were determined, and the expression of irisin and other proteins associated with AMPK/SIRT1/PGC-1α signal pathway, autophagy, and apoptosis was evaluated. Compared with the N group, the cells from the H group revealed lower proliferation, GSIS, and expression of irisin and proteins associated with AMPK/SIRT1/PGC-1α signal pathway and autophagy, but higher expression of proteins associated with apoptosis; in contrast, metformin could significantly rescue lower cell proliferation, GSIS, and expression of proteins associated with AMPK/SIRT1/PGC-1α signal pathway and autophagy, as well as irisin, and suppress apoptosis in high-glucose environment. Meanwhile, autophagy inhibitor CQ and SIRT1 inhibitor Ex527 can block above functions of metformin. Therefore, metformin can promote INS-1 cell proliferation, enhance GSIS, and suppress apoptosis by activating AMPK/SIRT1/PGC-1α signal pathway, up-regulating irisin expression, and inducing autophagy in INS-1 cells in high-glucose environment.

Indexed as

AMPK/SIRT1/PGC‐1α signal pathwayapoptosisautophagyINS‐1irisin

Identifiers

PMID31139382
PMCPMC6526663
OpenAlexW2929227384

What OpenQuestion holds

Textmetadata
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.