AI Article Synopsis

  • Pathological cardiac hypertrophy leads to reduced heart contractility due to an energy deficit from metabolic issues, especially in glucose metabolism.
  • This study examines D-Allose, a rare sugar, for its potential to restore metabolic balance and reverse cardiac hypertrophy by treating isolated neonatal rat heart cells with it while stimulating them with phenylephrine.
  • Results show D-Allose significantly reduced cardiomyocyte size and remodeling markers, decreased intracellular glucose levels, and inhibited glycolysis, also demonstrating effectiveness in mice with ISO-induced cardiac hypertrophy by reducing related markers with minimal impact on heart wall thickness.

Article Abstract

The hallmark of pathological cardiac hypertrophy is the decline in myocardial contractility caused by an energy deficit resulting from metabolic abnormalities, particularly those related to glucose metabolism. Here, we aim to explore whether D-Allose, a rare sugar that utilizes the same transporters as glucose, may restore metabolic equilibrium and reverse cardiac hypertrophy. Isolated neonatal rat cardiomyocytes were stimulated with phenylephrine and treated with D-Allose simultaneously for 48 h. D-Allose treatment resulted in a pronounced reduction in cardiomyocyte size and cardiac remodelling markers accompanied with a dramatic reduction in the level of intracellular glucose in phenylephrine-stimulated cells. The metabolic flux analysis provided further insights revealing that D-Allose exerted a remarkable inhibition of glycolysis as well as glycolytic capacity. Furthermore, in mice subjected to a 14-day continuous infusion of isoproterenol (ISO) to induce cardiac hypertrophy, D-Allose treatment via drinking water notably reduced ISO-induced cardiac hypertrophy and remodelling markers, with minimal effects on ventricular wall thickness observed in echocardiographic analyses. These findings indicate that D-Allose has the ability to attenuate the progression of cardiomyocyte hypertrophy by decreasing intracellular glucose flux and inhibiting glycolysis.

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http://dx.doi.org/10.1016/j.jphs.2024.08.002DOI Listing

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