Evidence map›Paper›PMID 32673151›Full record

ArticleIslets2020

Melatonin protects INS-1 pancreatic β-cells from apoptosis and senescence induced by glucotoxicity and glucolipotoxicity.

Yu Hee Lee, Hye Sook Jung, Min Jeong Kwon, Jung Eun Jang, Tae Nyun Kim, Soon Hee Lee, Mi-Kyung Kim, Jeong Hyun Park

Open access · bronzeAbstract read
In one paragraph

Article in Islets, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Melatonin in animal husbandry: functions and applications.Frontiers in veterinary science · 2024
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Diabetes and SARS-CoV-2-Is There a Mutual Connection?Frontiers in cell and developmental biology · 2022
    Review
  14. Control of Mesenchymal Stromal Cell Senescence by Tryptophan Metabolites.International journal of molecular sciences · 2021
    Review
  15. Review
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

8 authors at 2 institutions in 1 country.

Yu Hee LeeDepartment of Internal Medicine, College of Medicine, Inje University , Busan, Republic of Korea.
Hye Sook JungPaik Institute for Clinical Research, Inje University , Busan, Republic of Korea.
Min Jeong KwonDepartment of Internal Medicine, College of Medicine, Inje University , Busan, Republic of Korea.ORCID 0000-0002-9616-870X
Jung Eun JangDepartment of Internal Medicine, College of Medicine, Inje University , Busan, Republic of Korea.
Tae Nyun KimDepartment of Internal Medicine, College of Medicine, Inje University , Busan, Republic of Korea.ORCID 0000-0001-6568-2469
Soon Hee LeeDepartment of Internal Medicine, College of Medicine, Inje University , Busan, Republic of Korea.ORCID 0000-0003-4776-0501
Mi-Kyung KimDepartment of Internal Medicine, College of Medicine, Inje University , Busan, Republic of Korea.
Jeong Hyun ParkDepartment of Internal Medicine, College of Medicine, Inje University , Busan, Republic of Korea.
Inje University · KRInje University Busan Paik Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionMelatonin is a hormone known as having very strong anti-oxidant property. Senescence is a biological state characterized by the loss of cell replication and the changes consisting of a pro-inflammatory phenotype, leading to Senescence Associated Secretory Phenotype (SASP) which is now regarded as one of the fundamental processes of many degenerative diseases. Increased cell division count induces cell senescence via DNA damage in response to elevated Reactive Oxygen Species (ROS). We wanted to test whether melatonin could reduce apoptosis and stress induced premature pancreatic β-cell senescence induced by glucotoxicity and glucolipotoxicity. MATERIALS AND

methodCultured rodent pancreatic β-cell line (INS-1 cell) was used. Glucotoxicity (HG: hyperglycemia) and glucolipotoxicity (HGP: hyperglycemia with palmitate) were induced by hyperglycemia and the addition of palmitate. The degrees of the senescence were measured by SA-β-Gal and P16

resultsCultured INS-1 cells in HG and HGP conditions revealed accelerated senescence, increased apoptosis, cell cycle arrest, compromised endogenous anti-oxidant defense, and impaired glucose-stimulated insulin secretion. Melatonin decreased apoptosis and expressions of proteins related to senescence, increase the endogenous anti-oxidant defense, and improved glucose-stimulated insulin secretion.

conclusionMelatonin protected pancreatic β-cell from apoptosis, decreased expressions of the markers related to the accelerated senescence, and improved the biological deteriorations induced by glucotoxicity and glucolipotoxicity.

Indexed as

AnimalsApoptosisBlotting, WesternCell CycleCell Line, TumorCellular SenescenceHyperglycemiaInsulinInsulin-Secreting CellsMelatoninRatsInsulinMelatoninglucolipotoxicityglucotoxicityMelatoninpancreatic β-cellSenescence

Identifiers

PMID32673151
PMCPMC7527021
OpenAlexW3043337191

What OpenQuestion holds

Textmetadata
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.