Evidence map›Paper›PMID 21886784›Full record

ArticlePloS one2011

Ablation of TSC2 enhances insulin secretion by increasing the number of mitochondria through activation of mTORC1.

Maki Koyanagi, Shun-ichiro Asahara, Tomokazu Matsuda, Naoko Hashimoto, Yutaka Shigeyama, Yuki Shibutani, Ayumi Kanno, Megumi Fuchita, Tomoko Mikami, Tetsutya Hosooka and 8 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

41 citing papers in PubMed, 69 citations in OpenAlex.

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  14. Unraveling the multifaceted nature of the nuclear function of mTOR.Biochimica et biophysica acta. Molecular cell research · 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

18 authors at 6 institutions in 1 country.

Maki KoyanagiDivision of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, Kobe, Japan.
Shun-ichiro Asahara
Tomokazu Matsuda
Naoko Hashimoto
Yutaka Shigeyama
Yuki Shibutani
Ayumi Kanno
Megumi Fuchita
Tomoko Mikami
Tetsutya Hosooka
Hiroshi Inoue
Michihiro Matsumoto
Masato Koike
Yasuo Uchiyama
Tetsuo Noda
Susumu Seino
Masato Kasuga
Yoshiaki Kido
Kobe University · JPHyogo University of Health Sciences · JPJuntendo University · JPNational Center for Global Health and Medicine · JPJapanese Foundation For Cancer Research · JPKanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimWe previously found that chronic tuberous sclerosis protein 2 (TSC2) deletion induces activation of mammalian target of rapamycin Complex 1 (mTORC1) and leads to hypertrophy of pancreatic beta cells from pancreatic beta cell-specific TSC2 knockout (βTSC2(-/-)) mice. The present study examines the effects of TSC2 ablation on insulin secretion from pancreatic beta cells.

methodsIsolated islets from βTSC2(-/-) mice and TSC2 knockdown insulin 1 (INS-1) insulinoma cells treated with small interfering ribonucleic acid were used to investigate insulin secretion, ATP content and the expression of mitochondrial genes.

resultsActivation of mTORC1 increased mitochondrial DNA expression, mitochondrial density and ATP production in pancreatic beta cells of βTSC2(-/-) mice. In TSC2 knockdown INS-1 cells, mitochondrial DNA expression, mitochondrial density and ATP production were increased compared with those in control INS-1 cells, consistent with the phenotype of βTSC2(-/-) mice. TSC2 knockdown INS-1 cells also exhibited augmented insulin secretory response to glucose. Rapamycin inhibited mitochondrial DNA expression and ATP production as well as insulin secretion in response to glucose. Thus, βTSC2(-/-) mice exhibit hyperinsulinemia due to an increase in the number of mitochondria as well as enlargement of individual beta cells via activation of mTORC1.

conclusionActivation of mTORC1 by TSC2 ablation increases mitochondrial biogenesis and enhances insulin secretion from pancreatic beta cells.

Indexed as

Gene DeletionAnimalsCell LineGene Knockdown TechniquesGlucoseInsulinInsulin-Secreting CellsInsulin SecretionMechanistic Target of Rapamycin Complex 1MiceMitochondriaMultiprotein ComplexesOrgan SpecificityProteinsSirolimusTOR Serine-Threonine KinasesGlucoseInsulinMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesProteinsSirolimusTOR Serine-Threonine KinasesTsc2 protein, mouseTuberous Sclerosis Complex 2 ProteinTumor Suppressor Proteins

Identifiers

PMID21886784
PMCPMC3158755
OpenAlexW2036021095

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.