Evidence map›Paper›PMID 31767891›Full record

ArticleScientific reports2019

Kisspeptin-Activated Autophagy Independently Suppresses Non-Glucose-Stimulated Insulin Secretion from Pancreatic β-Cells.

Chien Huang, Hao-Yi Wang, Mu-En Wang, Meng-Chieh Hsu, Yi-Hsieng Samuel Wu, Yi-Fan Jiang, Leang-Shin Wu, De-Shien Jong, Chih-Hsien Chiu

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

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

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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

9 authors at 2 institutions in 2 countries.

Chien HuangLaboratory of Animal Physiology, Department of Animal Science and Technology, National Taiwan University, Taipei, 10617, Taiwan.
Hao-Yi WangLaboratory of Animal Physiology, Department of Animal Science and Technology, National Taiwan University, Taipei, 10617, Taiwan.
Mu-En WangLaboratory of Animal Physiology, Department of Animal Science and Technology, National Taiwan University, Taipei, 10617, Taiwan.
Meng-Chieh HsuLaboratory of Animal Physiology, Department of Animal Science and Technology, National Taiwan University, Taipei, 10617, Taiwan.
Yi-Hsieng Samuel WuLaboratory of Animal Physiology, Department of Animal Science and Technology, National Taiwan University, Taipei, 10617, Taiwan.
Yi-Fan JiangGraduate Institute of Molecular and Comparative Pathobiology, School of Medicine, National Taiwan University, Taipei, 10617, Taiwan.
Leang-Shin WuLaboratory of Animal Physiology, Department of Animal Science and Technology, National Taiwan University, Taipei, 10617, Taiwan.
De-Shien JongLaboratory of Animal Physiology, Department of Animal Science and Technology, National Taiwan University, Taipei, 10617, Taiwan.
Chih-Hsien ChiuLaboratory of Animal Physiology, Department of Animal Science and Technology, National Taiwan University, Taipei, 10617, Taiwan. chiuchihhsien@ntu.edu.tw.
National Taiwan University · TWDuke Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have demonstrated the important role of kisspeptin in impaired glucose-stimulated insulin secretion (GSIS). In addition, it was reported that the activation of autophagy in pancreatic β-cells decreases insulin secretion by selectively degrading insulin granules. However, it is currently unknown whether kisspeptin suppresses GSIS in β-cells by activating autophagy. To investigate the involvement of autophagy in kisspeptin-regulated insulin secretion, we overexpressed Kiss1 in NIT-1 cells to mimic the long-term exposure of pancreatic β-cells to kisspeptin during type 2 diabetes (T2D). Interestingly, our data showed that although kisspeptin potently decreases the intracellular proinsulin and insulin ((pro)insulin) content and insulin secretion of NIT-1 cells, autophagy inhibition using bafilomycin A1 and Atg5 siRNAs only rescues basal insulin secretion, not kisspeptin-impaired GSIS. We also generated a novel in vivo model to investigate the long-term exposure of kisspeptin by osmotic pump. The in vivo data demonstrated that kisspeptin lowers GSIS and (pro)insulin levels and also activated pancreatic autophagy in mice. Collectively, our data demonstrated that kisspeptin suppresses both GSIS and non-glucose-stimulated insulin secretion of pancreatic β-cells, but only non-glucose-stimulated insulin secretion depends on activated autophagic degradation of (pro)insulin. Our study provides novel insights for the development of impaired insulin secretion during T2D progression.

Indexed as

AnimalsAutophagyCell LineDiabetes Mellitus, Type 2Genes, ReporterGlucoseInsulinInsulin-Secreting CellsKisspeptinsMaleMiceMice, Inbred C57BLMice, Inbred NODMice, TransgenicProinsulinRecombinant ProteinsGlucoseInsulinKiss1 protein, mouseKisspeptinsProinsulinRecombinant Proteins

Identifiers

PMID31767891
PMCPMC6877614
OpenAlexW2991319152

What OpenQuestion holds

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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.