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October 10, 2025Circulation Research

Abstract Wed097: Metabolic Syndrome in Rodents Activates β-adrenergic Receptor Signaling Concealing Defects in Cardiac Performance

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Key result

Diet-induced metabolic syndrome masks underlying cardiac dysfunction via beta-adrenergic signaling in preclinical models.

Population

C57Bl/6 wild-type mice and β1- and β2-AR knockout (βAR-KO) mice

Comparison

Western diet for >4 months to induce Metabolic… vs Regular chow (Ctrl)

Design

Preclinical

Follow-up

>4 months

Authors

GPGiulia PiccininiUniversity of ParmaDCDaniel O. CervantesNew York Medical CollegeMSMichael SunSUNY Upstate Medical University

Discussion

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Implication

Metabolic syndrome induces compensatory β-adrenergic receptor activation in the heart, which masks underlying defects in cardiac and cardiomyocyte function.

Key Points

  • Metabolic syndrome exacerbates heart rate variations, indicating sympathoexcitation in the heart.
  • Inhibition of β-adrenergic receptors normalizes heart rates in mice with metabolic syndrome.
  • Echocardiographic analysis shows no baseline differences in cardiac function until β-AR blockade.
  • Left ventricular myocytes from metabolic syndrome mice exhibit increased cell shortening, revealing hidden cardiac dysfunction.

Structured PICO

P
Population
Male and female C57Bl/6 and βAR-KO mice subjected to chronic Western diet (>4 months) to induce metabolic syndrome.
I
Intervention
Western diet (WesD) for >4 months to induce Metabolic Syndrome, with or without acute β-adrenergic receptor blockade using propranolol
C
Comparator
Regular chow (Ctrl)
O
Outcome
Cardiac function (ejection fraction, isovolumic relaxation time) and cardiomyocyte function (fractional cell shortening, relaxation kinetics)surrogate

Metabolic syndrome induces compensatory β-adrenergic receptor activation in the heart, which masks underlying defects in cardiac and cardiomyocyte function.

Cite This Study

Piccinini et al. (2025) studied Metabolic Syndrome. Western diet (WesD) vs. Regular chow (Ctrl) was evaluated on Cardiac performance (ejection fraction, isovolumic relaxation time, fractional cell shortening). In mice, metabolic syndrome induced by a Western diet activated β-adrenergic receptor signaling, concealing underlying defects in cardiac function such as reduced ejection fraction.

synapsesocial.com/papers/68e861a57ef2f04ca37e47b9https://doi.org/10.1161/res.137.suppl_1.wed097
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1The Role of Reactive Oxygen Species in β-Adrenergic Signaling in Cardiomyocytes from Mice with the Metabolic Syndrome2016 · 25 citations
  2. 2Altered β-Adrenergic System, Cardiac Dysfunction, and Lethal Arrhythmia in a Rat Model of Metabolic Syndrome2025 · 1 citations
  3. 3A custom analysis of R-R interval properties reveals alterations in the brain-heart axis in experimental animals with metabolic syndrome2025 · 1 citations
  4. 4Profiling of cardiac β-adrenoceptor subtypes in the cardiac left ventricle of rats with metabolic syndrome: Comparison with streptozotocin-induced diabetic rats2015 · 28 citations
  5. 5Cardiac ß-adrenoceptor expression is markedly depressed in Ossabaw swine model of cardiometabolic risk2011 · 15 citations