Life (Dec 2020)

β-Catenin Regulates Cardiac Energy Metabolism in Sedentary and Trained Mice

  • Volodymyr V. Balatskyi,
  • Oksana L. Palchevska,
  • Lina Bortnichuk,
  • Ana-Maria Gan,
  • Anna Myronova,
  • Larysa L. Macewicz,
  • Viktor O. Navrulin,
  • Lesya V. Tumanovska,
  • Adam Olichwier,
  • Pawel Dobrzyn,
  • Oksana O. Piven

DOI
https://doi.org/10.3390/life10120357
Journal volume & issue
Vol. 10, no. 12
p. 357

Abstract

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The role of canonical Wnt signaling in metabolic regulation and development of physiological cardiac hypertrophy remains largely unknown. To explore the function of β-catenin in the regulation of cardiac metabolism and physiological cardiac hypertrophy development, we used mice heterozygous for cardiac-specific β-catenin knockout that were subjected to a swimming training model. β-Catenin haploinsufficient mice subjected to endurance training displayed a decreased β-catenin transcriptional activity, attenuated cardiomyocytes hypertrophic growth, and enhanced activation of AMP-activated protein kinase (AMPK), phosphoinositide-3-kinase–Akt (Pi3K–Akt), and mitogen-activated protein kinase/extracellular signal-regulated kinases 1/2 (MAPK/Erk1/2) signaling pathways compared to trained wild type mice. We further observed an increased level of proteins involved in glucose aerobic metabolism and β-oxidation along with perturbed activity of mitochondrial oxidative phosphorylation complexes (OXPHOS) in trained β-catenin haploinsufficient mice. Taken together, Wnt/β-catenin signaling appears to govern metabolic regulatory programs, sustaining metabolic plasticity in adult hearts during the adaptation to endurance training.

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