Evidence map›Paper›PMID 34307343›Full record

ArticleFrontiers in cell and developmental biology2021

GLP-1-Induced AMPK Activation Inhibits PARP-1 and Promotes LXR-Mediated ABCA1 Expression to Protect Pancreatic β-Cells Against Cholesterol-Induced Toxicity Through Cholesterol Efflux.

Rao Li, Xulong Sun, Pengzhou Li, Weizheng Li, Lei Zhao, Liyong Zhu, Shaihong Zhu

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

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

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  18. The Pathogenic Role of Long Non-coding RNA H19 in AtherosclerosisFrontiers in cardiovascular medicine · 2021
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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 3 institutions in 1 country.

Rao LiDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital, Central South University, Changsha, China.
Xulong SunDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital, Central South University, Changsha, China.
Pengzhou LiDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital, Central South University, Changsha, China.
Weizheng LiDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital, Central South University, Changsha, China.
Lei ZhaoDepartment of General Surgery, First Affiliated Hospital of University of South China, Hengyang, China.
Liyong ZhuDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital, Central South University, Changsha, China.
Shaihong ZhuDepartment of Gastrointestinal Surgery, The Third Xiangya Hospital, Central South University, Changsha, China.
Central South University · CNThird Xiangya Hospital · CNFirst Affiliated Hospital of University of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T2DM (Type 2 diabetes) is a complex, chronic disease characterized as insulin resistance and islet β-cell dysfunction. Bariatric surgeries such as Roux-en-Y gastric bypass (RYGB) surgery and laparoscopic sleeve gastrectomy (LSG) have become part of a critical treatment regimen in the treatment of obesity and T2DM. Moreover, GLP-1 increase following bariatric surgery has been regarded as a significant event in bariatric surgery-induced remission of T2DM. In this study, a high concentration cholesterol-induced lipotoxicity was observed in INS-1 cells, including inhibited cell viability and insulin secretion. Enhanced cell apoptosis and inhibited cholesterol efflux from INS-1 cells; meanwhile, ABCA1 protein level was decreased by cholesterol stimulation. Cholesterol-induced toxicity and ABCA1 downregulation were attenuated by GLP-1 agonist EX-4. GLP-1 induced AMPK phosphorylation during the protection against cholesterol-induced toxicity. Under cholesterol stimulation, GLP-1-induced AMPK activation inhibited PARP-1 activity, therefore attenuating cholesterol-induced toxicity in INS-1 cells. In INS-1 cells, PARP-1 directly interacted with LXR, leading to the poly(ADP-ribosyl)ation of LXRα and downregulation of LXR-mediated ABCA1 expression. In the STZ-induced T2DM model in rats, RYGB surgery or EX-4 treatment improved the glucose metabolism and lipid metabolism in rats through GLP-1 inhibition of PARP-1 activity. In conclusion, GLP-1 inhibits PARP-1 to protect islet β cell function against cholesterol-induced toxicity

Indexed as

ABCA1GLP-1PARP-1T2DM (type 2 diabetes)β-cell

Identifiers

PMID34307343
PMCPMC8292745
OpenAlexW3119546189

What OpenQuestion holds

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Registered trials

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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.