Evidence map›Paper›PMID 21115496›Full record

ArticleThe Journal of biological chemistry2011

Mitochondrial dysfunction and increased reactive oxygen species impair insulin secretion in sphingomyelin synthase 1-null mice.

Masato Yano, Ken Watanabe, Tadashi Yamamoto, Kazutaka Ikeda, Takafumi Senokuchi, Meihong Lu, Tsuyoshi Kadomatsu, Hiroto Tsukano, Masahito Ikawa, Masaru Okabe and 9 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.

  1. Pooled it
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  15. Effect of Total SMS Activity on LDL Catabolism in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2023
    Article
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  17. Article
  18. Review
  19. Review
  20. Sphingolipids in Atherosclerosis: Chimeras in Structure and Function.International journal of molecular sciences · 2022
    Review

23 more citing papers are in PubMed but not listed here.

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

19 authors at 7 institutions in 2 countries.

Masato YanoDepartment of Molecular Genetics, Faculty of Life Sciences, Kumamoto University, Kumamoto 860-8556, Japan. myano@gpo.kumamoto-u.ac.jp
Ken Watanabe
Tadashi Yamamoto
Kazutaka Ikeda
Takafumi Senokuchi
Meihong Lu
Tsuyoshi Kadomatsu
Hiroto Tsukano
Masahito Ikawa
Masaru Okabe
Shohei Yamaoka
Toshiro Okazaki
Hisanori Umehara
Tomomi Gotoh
Wen-Jie Song
Koichi Node
Ryo Taguchi
Kazuya Yamagata
Yuichi Oike
Laboratory of Molecular Genetics · PLKumamoto University · JPNational Center for Geriatrics and Gerontology · JPSaga University · JPThe University of Tokyo · JPTottori University · JPKanazawa Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sphingomyelin synthase 1 (SMS1) catalyzes the conversion of ceramide to sphingomyelin. Here, we generated and analyzed SMS1-null mice. SMS1-null mice exhibited moderate neonatal lethality, reduced body weight, and loss of fat tissues mass, suggesting that they might have metabolic abnormality. Indeed, analysis on glucose metabolism revealed that they showed severe deficiencies in insulin secretion. Isolated mutant islets exhibited severely impaired ability to release insulin, dependent on glucose stimuli. Further analysis indicated that mitochondria in mutant islet cells cannot up-regulate ATP production in response to glucose. We also observed additional mitochondrial abnormalities, such as hyperpolarized membrane potential and increased levels of reactive oxygen species (ROS) in mutant islets. Finally, when SMS1-null mice were treated with the anti-oxidant N-acetyl cysteine, we observed partial recovery of insulin secretion, indicating that ROS overproduction underlies pancreatic β-cell dysfunction in SMS1-null mice. Altogether, our data suggest that SMS1 is important for controlling ROS generation, and that SMS1 is required for normal mitochondrial function and insulin secretion in pancreatic β-cells.

Indexed as

AnimalsAntioxidantsGlucoseInsulinInsulin-Secreting CellsInsulin SecretionMiceMice, KnockoutMitochondriaMutationPhenotypeReactive Oxygen SpeciesTransferases (Other Substituted Phosphate Groups)AntioxidantsGlucoseInsulinReactive Oxygen SpeciesSgms1 protein, mouseTransferases (Other Substituted Phosphate Groups)

Identifiers

PMID21115496
PMCPMC3030399
OpenAlexW2031401392

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.