Evidence map›Paper›PMID 34205555›Full record

ArticleCells2021

TRPV1 Activation by Capsaicin Mediates Glucose Oxidation and ATP Production Independent of Insulin Signalling in Mouse Skeletal Muscle Cells.

Parisa Vahidi Ferdowsi, Kiran D K Ahuja, Jeffrey M Beckett, Stephen Myers

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Role of TRP Channels in Cancer-Induced Bone Pain.International journal of molecular sciences · 2025
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Phenolic Compounds and Capsaicinoids in ThreeMolecules (Basel, Switzerland) · 2023
    Article
  17. Review
  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

4 authors at 1 institution in 2 countries.

Parisa Vahidi FerdowsiSchool of Health Sciences, College of Health and Medicine, University of Tasmania, Newnham Drive, Launceston, TAS 7248, Australia.
Kiran D K AhujaSchool of Health Sciences, College of Health and Medicine, University of Tasmania, Newnham Drive, Launceston, TAS 7248, Australia.ORCID 0000-0002-0323-4692
Jeffrey M BeckettSchool of Health Sciences, College of Health and Medicine, University of Tasmania, Newnham Drive, Launceston, TAS 7248, Australia.ORCID 0000-0002-2911-0313
Stephen MyersSchool of Health Sciences, College of Health and Medicine, University of Tasmania, Newnham Drive, Launceston, TAS 7248, Australia.ORCID 0000-0003-4793-3820
University of Tasmania · AU

Funding

Clifford Craig Foundation 190
6 · The paper itself

Abstract

backgroundInsulin resistance (IR), a key characteristic of type 2 diabetes (T2DM), is manifested by decreased insulin-stimulated glucose transport in target tissues. Emerging research has highlighted transient receptor potential cation channel subfamily V member (TRPV1) activation by capsaicin as a potential therapeutic target for these conditions. However, there are limited data on the effects of capsaicin on cell signalling molecules involved in glucose uptake.

methodsC2C12 cells were cultured and differentiated to acquire the myotube phenotype. The activation status of signalling molecules involved in glucose metabolism, including 5' adenosine monophosphate-activated protein kinase (AMPK), calcium/calmodulin-dependent protein kinase 2 (CAMKK2), extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), protein kinase B (AKT), and src homology phosphatase 2 (SHP2), was examined. Finally, activation of CAMKK2 and AMPK, and glucose oxidation and ATP levels were measured in capsaicin-treated cells in the presence or absence of TRPV1 antagonist (SB-452533).

resultsCapsaicin activated cell signalling molecules including CAMKK2 and AMPK leading to increased glucose oxidation and ATP generation independent of insulin in the differentiated C2C12 cells. Pharmacological inhibition of TRPV1 diminished the activation of CAMKK2 and AMPK as well as glucose oxidation and ATP production. Moreover, we observed an inhibitory effect of capsaicin in the phosphorylation of ERK1/2 in the mouse myotubes.

conclusionOur data show that capsaicin-mediated stimulation of TRPV1 in differentiated C2C12 cells leads to activation of CAMKK2 and AMPK, and increased glucose oxidation which is concomitant with an elevation in intracellular ATP level. Further studies of the effect of TRPV1 channel activation by capsaicin on glucose metabolism could provide novel therapeutic utility for the management of IR and T2DM.

Indexed as

Adenosine TriphosphateAnimalsCapsaicinCell LineGlucoseInsulinMAP Kinase Signaling SystemMiceMuscle, SkeletalOxidation-ReductionTRPV Cation ChannelsAdenosine TriphosphateCapsaicinGlucoseInsulinTRPV1 protein, mouseTRPV Cation ChannelsATPCAMKK2capsaicinERK1/2glucose oxidationskeletal muscleTRPV1

Identifiers

PMID34205555
PMCPMC8234135
OpenAlexW3176479092

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.