Evidence map›Paper›PMID 23137106›Full record

ArticleCardiovascular diabetology2012

Telmisartan ameliorates insulin sensitivity by activating the AMPK/SIRT1 pathway in skeletal muscle of obese db/db mice.

Asuka Shiota, Michio Shimabukuro, Daiju Fukuda, Takeshi Soeki, Hiromi Sato, Etsuko Uematsu, Yoichiro Hirata, Hirotsugu Kurobe, Norikazu Maeda, Hiroshi Sakaue and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.4field-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

28 citing papers in PubMed, 63 citations in OpenAlex.

  1. Trial
  2. Prevention of metabolic disorders with telmisartan and indapamide in a Chinese population with high-normal blood pressure.Hypertension research : official journal of the Japanese Society of Hypertension · 2015
    Trial
  3. Trial
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Nutrients · 2021
    Article
  16. Review
  17. Observational
  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

13 authors at 3 institutions in 1 country.

Asuka ShiotaDepartment of Cardio-Diabetes Medicine, University of Tokushima Graduate School of Health Biosciences, 3-18-15 Kuramoto, Tokushima 770-8503, Japan.
Michio Shimabukuro
Daiju Fukuda
Takeshi Soeki
Hiromi Sato
Etsuko Uematsu
Yoichiro Hirata
Hirotsugu Kurobe
Norikazu Maeda
Hiroshi Sakaue
Hiroaki Masuzaki
Iichiro Shimomura
Masataka Sata
Tokushima University · JPOsaka University · JPUniversity of the Ryukyus · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTelmisartan is a well-established angiotensin II type 1 receptor blocker that improves insulin sensitivity in animal models of obesity and insulin resistance, as well as in humans. Telmisartan has been reported to function as a partial agonist of the peroxisome proliferator-activated receptor (PPAR) γ, which is also targeted by the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase (SIRT1). Here, we investigated the pathways through which telmisartan acts on skeletal muscle, in vitro as well as in vivo.

methodsNine-week-old male db/db mice were fed a 60% high-fat diet, with orally administrated either vehicle (carboxymethyl-cellulose, CMC), 5 mg/kg telmisartan, or 5 mg/kg telmisartan and 1 mg/kg GW9662, a selective irreversible antagonist of PPARγ, for 5 weeks. Effects of telmisartan on Sirt1 mRNA, AMPK phosphorylation, and NAD+/NADH ratio were determined in C2C12 cultured myocytes. RESULTS AND DISCUSSION: Telmisartan treatment improved insulin sensitivity in obese db/db mice fed a high-fat diet and led to reduction in the size of hypertrophic pancreatic islets in these mice. Moreover, in vitro treatment with telmisartan led to increased expression of Sirt1 mRNA in C2C12 skeletal muscle cells; the increase in Sirt1 mRNA in telmisartan-treated C2C12 myoblasts occurred concomitantly with an increase in AMPK phosphorylation, an increase in NAD+/NADH ratio, and increases in the mRNA levels of PGC1α, FATP1, ACO, and GLUT4.

conclusionsOur results indicate that telmisartan acts through a PPARγ-independent pathway, but at least partially exerts its effects by acting directly on skeletal muscle AMPK/SIRT1 pathways.

Indexed as

AdipocytesAdministration, OralAMP-Activated Protein KinasesAngiotensin II Type 1 Receptor BlockersAnilidesAnimalsBenzimidazolesBenzoatesCell LineDiabetes MellitusDiet, High-FatDisease Models, AnimalDose-Response Relationship, DrugEnzyme ActivationFatty Acid Transport ProteinsGlucose Transporter Type 42-chloro-5-nitrobenzanilideAMP-Activated Protein KinasesAngiotensin II Type 1 Receptor BlockersAnilidesBenzimidazolesBenzoatesFatty Acid Transport ProteinsGlucose Transporter Type 4InsulinNADPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPAR gammaPpargc1a protein, mouseRNA, MessengerSirt1 protein, mouseSirtuin 1Slc27a1 protein, mouseSlc2a4 protein, mouseTelmisartanTrans-ActivatorsTranscription Factors

Identifiers

PMID23137106
PMCPMC3527353
OpenAlexW2136527848

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.