Evidence map›Paper›PMID 15760936›Full record

ArticleThe Journal of physiology2005

Leptin repletion restores depressed {beta}-adrenergic contractility in ob/ob mice independently of cardiac hypertrophy.

Khalid M Minhas, Shakil A Khan, Shubha V Y Raju, Alexander C Phan, Daniel R Gonzalez, Mike W Skaf, Kwangho Lee, Ankit D Tejani, Anastasios P Saliaris, Anastasies P Saliaris and 5 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Leptin as a Key between Obesity and Cardiovascular Disease.Journal of obesity & metabolic syndrome · 2020
    Review
  5. Leptin Levels are Associated with Subclinical Cardiac Dysfunction in Obese Adolescents.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Impaired cardiac function in leptin-deficient mice.Current hypertension reports · 2008
    Review
  18. Cardiac remodeling in obesity.Physiological reviews · 2008
    Review
  19. Article
  20. Review
4 · The record

Corrections and comments

  • Erratum issued
    Saliaris, Anastasies P [corrected to Saliaris, Anastasios P]
5 · Who and what money

Authors and funding

15 authors at 1 institution in 1 country.

Khalid M MinhasThe Johns Hopkins Medical Institutions, Cardiology Division, 720 Rutland Avenue, Ross 1059, Baltimore, MD 21205, USA.
Shakil A Khan
Shubha V Y Raju
Alexander C Phan
Daniel R Gonzalez
Mike W Skaf
Kwangho Lee
Ankit D Tejani
Anastasios P Saliaris
Anastasies P Saliaris
Lili A Barouch
Christopher P O'Donnell
Charles W Emala
Dan E Berkowitz
Joshua M Hare
Johns Hopkins University · US

Funding

OXIDATIVE STRESS IN HEART FAILURE: MECHANISMSR01HL065455 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARE, JOSHUA M · 2000 to 2008
$2.6M
Leptin Signaling in Cardiac HypertrophyK08HL076220 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BAROUCH, LILI A · 2004 to 2008
$666k
NHLBI NIH HHS K08 HL076220NHLBI NIH HHS KO8 HL-076220NHLBI NIH HHS R01 HL065455NHLBI NIH HHS R01 HL-65455
6 · The paper itself

Abstract

Impaired leptin signalling in obesity is increasingly implicated in cardiovascular pathophysiology. To explore mechanisms for leptin activity in the heart, we hypothesized that physiological leptin signalling participates in maintaining cardiac beta-adrenergic regulation of excitation-contraction coupling. We studied 10-week-old (before development of cardiac hypertrophy) leptin-deficient (ob/ob, n=12) and C57Bl/6 (wild-type (WT), n=15) mice at baseline and after recombinant leptin infusion (0.3 mg kg-1 day-1 for 28 days, n=6 in each group). Ob/ob-isolated myocytes had attenuated sarcomere shortening and calcium transients ([Ca2+]i) versus WT (P<0.01 for both) following stimulation of the beta-receptor (with isoproterenol (isoprenaline)) or at the post-receptor level (with forskolin and dibutryl-cAMP). In addition, sarcoplasmic reticulum (SR) Ca2+ stores were depressed. Leptin replenishment in ob/ob mice restored each of these abnormalities towards normal without affecting gross (wall thickness) or microscopic (cell size) measures of cardiac architecture. Immunoblots revealed alterations of several proteins involved in excitation-contraction coupling in the ob/ob mice, including decreased abundance of Gsalpha-52 kDa, as well as alterations in the expression of Ca2+ cycling proteins (increased SR Ca2+-ATPase, and depressed phosphorylated phospholamban). In addition, protein kinase A (PKA) activity in ob/ob mice was depressed at baseline and correctable towards the activity found in WT with leptin repletion, a finding that could account for impaired beta-adrenergic responsiveness. Taken together, these data reveal a novel link between the leptin signalling pathway and normal cardiac function and suggest a mechanism by which leptin deficiency or resistance may lead to cardiac depression.

Indexed as

Adenylyl CyclasesAdrenergic beta-AgonistsAge FactorsAnimalsBlotting, WesternCalciumCardiomegalyCyclic AMPCyclic AMP-Dependent Protein KinasesIsoproterenolLeptinMiceMice, Inbred C57BLMice, ObeseMyocardial ContractionObesityAdenylyl CyclasesAdrenergic beta-AgonistsCalciumCyclic AMPCyclic AMP-Dependent Protein KinasesIsoproterenolLeptinleptin receptor, mouseReceptors, Adrenergic, betaReceptors, Leptin

Identifiers

PMID15760936
PMCPMC1464532
OpenAlexW2165961251

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.