Evidence map›Paper›PMID 21813874›Full record

ReviewAmerican journal of physiology. Regulatory, integrative and comparative physiology2011

Adaptive mechanisms to compensate for overnutrition-induced cardiovascular abnormalities.

Lakshmi Pulakat, Vincent G DeMarco, Sivakumar Ardhanari, Anand Chockalingam, Rukhsana Gul, Adam Whaley-Connell, James R Sowers

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Regulatory, integrative and comparative physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Inflammation in Metabolic Cardiomyopathy.Frontiers in cardiovascular medicine · 2021
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. The two faces of miR-29.Journal of cardiovascular medicine (Hagerstown, Md.) · 2015
    Review
  18. Overnutrition, mTOR signaling, and cardiovascular diseases.American journal of physiology. Regulatory, integrative and comparative physiology · 2014
    Review
  19. Review
  20. Review
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

7 authors at 3 institutions in 2 countries.

Lakshmi PulakatUniversity of Missouri School of Medicine, Department of Internal Medicine, Columbia, Missouri 65212, USA.
Vincent G DeMarco
Sivakumar Ardhanari
Anand Chockalingam
Rukhsana Gul
Adam Whaley-Connell
James R Sowers
Harry S. Truman Memorial Veterans' Hospital · USDiabetes Australia · AUUniversity of Missouri · US

Funding

ANG II OPPOSES INS MEDIATED VASORELAXATION &GLU UTILZAR01HL073101 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI SOWERS, JAMES RUSSELL · 2004 to 2013
$2.7M
Ang II and Overnutrition and Insulin resistance in Cardiovascular TissueR01HL107910 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI SOWERS, JAMES RUSSELL · 2011 to 2015
$1.8M
NHLBI NIH HHS R01 HL073101NHLBI NIH HHS R01 HL107910NHLBI NIH HHS R01 HL73101-01A1
6 · The paper itself

Abstract

In conditions of overnutrition, cardiac cells must cope with a multitude of extracellular signals generated by changes in nutrient load (glucose, amino acids, and lipids) and the hormonal milieu [increased insulin (INS), ANG II, and adverse cytokine/adipokine profile]. Herein, we review the diverse compensatory/adaptive mechanisms that counter the deleterious effects of excess nutrients and growth factors. We largely focus the discussion on evidence obtained from Zucker obese (ZO) and Zucker diabetic fatty (ZDF) rats, which are useful models to evaluate adaptive and maladaptive metabolic, structural, and functional cardiac remodeling. One adaptive mechanism present in the INS-resistant ZO, but absent in the diabetic ZDF heart, involves an interaction between the nutrient sensor kinase mammalian target of rapamycin complex 1 (mTORC1) and ANG II-type 2 receptor (AT2R). Recent evidence supports a cardioprotective role for the AT2R; for example, suppression of AT2R activation interferes with antihypertrophic/antifibrotic effects of AT1R blockade, and AT2R agonism improves cardiac structure and function. We propose a scenario, whereby mTORC1-signaling-mediated increase in AT2R expression in the INS-resistant ZO heart is a cardioprotective adaptation to overnutrition. In contrast to the ZO rat, heart tissues of ZDF rats do not show activation of mTORC1. We posit that such a lack of activation of the mTOR↔AT2R integrative pathway in cardiac tissue under conditions of obesity-induced diabetes may be a metabolic switch associated with INS deficiency and clinical diabetes.

Indexed as

Adaptation, PhysiologicalAnimalsCardiovascular DiseasesDisease Models, AnimalMetabolic SyndromeOvernutritionRatsRats, ZuckerReceptors, AngiotensinSignal TransductionTOR Serine-Threonine KinasesmTOR protein, ratReceptors, AngiotensinTOR Serine-Threonine Kinases

Identifiers

PMID21813874
PMCPMC3289980
OpenAlexW2017496399

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.