Evidence map›Paper›PMID 23426760›Full record

ArticleJournal of nuclear medicine : official publication, Society of Nuclear Medicine2013

Quantitative PET imaging detects early metabolic remodeling in a mouse model of pressure-overload left ventricular hypertrophy in vivo.

Min Zhong, Clayton E Alonso, Heinrich Taegtmeyer, Bijoy K Kundu

Open access · bronzeAbstract read
In one paragraph

Article in Journal of nuclear medicine : official publication, Society of Nuclear Medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.8field-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

40 citing papers in PubMed, 61 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. UCP1-dependent brown adipose activation accelerates cardiac metabolic remodeling and reduces initial hypertrophic and fibrotic responses to pathological stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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  6. Article
  7. Review
  8. Article
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  11. Metabolic remodeling precedes mTORC1-mediated cardiac hypertrophy.Journal of molecular and cellular cardiology · 2021
    Article
  12. Article
  13. Article
  14. Increased myocardialJournal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2020
    Article
  15. Article
  16. Multimodality Imaging of Inflammation and Ventricular Remodeling in Pressure-Overload Heart Failure.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2020
    Article
  17. Review
  18. Simultaneous determination of dynamic cardiac metabolism and function using PET/MRI.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2019
    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 2 institutions in 1 country.

Min ZhongDepartment of Physics, University of Virginia, Charlottesville, VA 22908, USA.
Clayton E Alonso
Heinrich Taegtmeyer
Bijoy K Kundu
University of Virginia · USTexas Medical Center · US

Funding

SWITCHING OF METABOLIC GENES IN UNLOADED HEARTR01HL061483 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI TAEGTMEYER, HEINRICH · 1999 to 2021
$6.2M
Metabolic remodeling precedes and triggers left ventricular remodeling in cardiacR21HL102627 · NHLBI · UNIVERSITY OF VIRGINIA · PI KUNDU, BIJOY K · 2010 to 2011
$408k
NHLBI NIH HHS R01 HL061483NHLBI NIH HHS R21 HL102627
6 · The paper itself

Abstract

unlabelledWe proposed that metabolic remodeling in the form of increased uptake of the myocardial glucose analog (18)F-FDG precedes and triggers the onset of severe contractile dysfunction in pressure-overload left ventricular hypertrophy in vivo. To test this hypothesis, we used a mouse model of transverse aortic constriction (TAC) together with PET and assessed serial changes in cardiac metabolism and function over 7 d.

methodsScans of 16 C57BL/6 male mice were obtained using a small-animal PET device under sevoflurane anesthesia. A 10-min transmission scan was followed by a 60-min dynamic (18)F-FDG PET scan with cardiac and respiratory gating. Blood glucose levels were measured before and after the emission scan. TAC and sham surgeries were performed after baseline imaging. Osmotic mini pumps containing either propranolol (5 mg/kg/d) or vehicle alone were implanted subcutaneously at the end of surgery. Subsequent scans were taken at days 1 and 7 after surgery. A compartment model, in which the blood input function with spillover and partial-volume corrections and the metabolic rate constants in a 3-compartment model are simultaneously estimated, was used to determine the net myocardial (18)F-FDG influx constant, Ki. The rate of myocardial glucose utilization, rMGU, was also computed. Estimations of the ejection fractions were based on the high-resolution gated PET images.

resultsMice undergoing TAC surgery exhibited an increase in the Ki (580%) and glucose utilization the day after surgery, indicating early adaptive response. On day 7, the ejection fraction had decreased by 24%, indicating a maladaptive response. Average Ki increases were not linearly associated with increases in rMGU. Ki exceeded rMGU by 29% in the TAC mice. TAC mice treated with propranolol attenuated the rate of (18)F-FDG uptake, diminished mismatch between Ki and rMGU (9%), and rescued cardiac function.

conclusionMetabolic maladaptation precedes the onset of severe contractile dysfunction. Both are prevented by treatment with propranolol. The early detection of metabolic remodeling may offer a metabolic target for modulation of hypertrophy.

Indexed as

Positron-Emission TomographyVentricular RemodelingAnimalsDisease Models, AnimalGlucoseHypertrophy, Left VentricularMaleMiceMice, Inbred C57BLModels, BiologicalPressureRespiratory-Gated Imaging TechniquesStroke VolumeTime FactorsGlucose

Identifiers

PMID23426760
PMCPMC3727159
OpenAlexW2129998919

What OpenQuestion holds

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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.