Evidence map›Paper›PMID 24551069›Full record

ArticlePloS one2014

Cinnamon extract enhances glucose uptake in 3T3-L1 adipocytes and C2C12 myocytes by inducing LKB1-AMP-activated protein kinase signaling.

Yan Shen, Natsumi Honma, Katsuya Kobayashi, Liu Nan Jia, Takashi Hosono, Kazutoshi Shindo, Toyohiko Ariga, Taiichiro Seki

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Glyoxalase 1 is a proadipogenic gene.The Journal of biological chemistry · 2025
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Cell-free supernatant ofFrontiers in microbiology · 2024
    Article
  10. Review
  11. Quercetin-3-Revista brasileira de farmacognosia : orgao oficial da Sociedade Brasileira de Farmacognosia · 2023
    Article
  12. Article
  13. A bioactive component ofToxicology research · 2022
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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.

Yan ShenDepartment of Chemistry and Life Science, Nihon University College of Bioresource Sciences, Nihon University Graduate School of Bioresource Sciences, Kanagawa, Japan.
Natsumi HonmaDepartment of Chemistry and Life Science, Nihon University College of Bioresource Sciences, Nihon University Graduate School of Bioresource Sciences, Kanagawa, Japan.
Katsuya KobayashiDepartment of Chemistry and Life Science, Nihon University College of Bioresource Sciences, Nihon University Graduate School of Bioresource Sciences, Kanagawa, Japan.
Liu Nan JiaSchool of Pharmacy, Nihon University, Chiba, Japan.
Takashi HosonoDepartment of Chemistry and Life Science, Nihon University College of Bioresource Sciences, Nihon University Graduate School of Bioresource Sciences, Kanagawa, Japan.
Kazutoshi ShindoDepartment of Food and Nutrition, Japan Women's University, Tokyo, Japan.
Toyohiko ArigaDepartment of Chemistry and Life Science, Nihon University College of Bioresource Sciences, Nihon University Graduate School of Bioresource Sciences, Kanagawa, Japan.
Taiichiro SekiDepartment of Chemistry and Life Science, Nihon University College of Bioresource Sciences, Nihon University Graduate School of Bioresource Sciences, Kanagawa, Japan.
Nihon University · JPJapan Women's University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously demonstrated that cinnamon extract (CE) ameliorates type 1 diabetes induced by streptozotocin in rats through the up-regulation of glucose transporter 4 (GLUT4) translocation in both muscle and adipose tissues. This present study was aimed at clarifying the detailed mechanism(s) with which CE increases the glucose uptake in vivo and in cell culture systems using 3T3-L1 adipocytes and C2C12 myotubes in vitro. Specific inhibitors of key enzymes in insulin signaling and AMP-activated protein kinase (AMPK) signaling pathways, as well as small interference RNA, were used to examine the role of these kinases in the CE-induced glucose uptake. The results showed that CE stimulated the phosphorylation of AMPK and acetyl-CoA carboxylase. An AMPK inhibitor and LKB1 siRNA blocked the CE-induced glucose uptake. We also found for the first time that insulin suppressed AMPK activation in the adipocyte. To investigate the effect of CE on type 2 diabetes in vivo, we further performed oral glucose tolerance tests and insulin tolerance tests in type 2 diabetes model rats administered with CE. The CE improved glucose tolerance in oral glucose tolerance tests, but not insulin sensitivity in insulin tolerance test. In summary, these results indicate that CE ameliorates type 2 diabetes by inducing GLUT4 translocation via the AMPK signaling pathway. We also found insulin antagonistically regulates the activation of AMPK.

Indexed as

3T3-L1 CellsAdipocytesAMP-Activated Protein KinasesAnimalsBody WeightCinnamomum zeylanicumDiabetes Mellitus, Type 2Disease Models, AnimalGene Knockdown TechniquesGlucoseGlucose Transporter Type 4InsulinInsulin ResistanceMaleMiceMuscle CellsAMP-Activated Protein KinasesGlucoseGlucose Transporter Type 4InsulinPlant ExtractsProtein Kinase InhibitorsProtein Serine-Threonine KinasesStk11 protein, mouse

Identifiers

PMID24551069
PMCPMC3925101
OpenAlexW1983017314

What OpenQuestion holds

Textmetadata
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.