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Cardiac phosphocreatine deficiency induced by GPA during postnatal development in rat

V Pelouch1, F Kolár, Z A Khuchua

  • 1Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic.

Insights

Chronic beta-guanidinopropionic acid (GPA) administration impairs developing rat heart function by altering energy metabolism and protein profiles. This study highlights the creatine kinase system's importance in cardiac health and growth.

Area of Science:

  • Cardiovascular Physiology
  • Biochemistry
  • Molecular Biology

Background:

  • Beta-guanidinopropionic acid (GPA) is a creatine analog that can disrupt cellular energy metabolism.
  • The developing heart is particularly vulnerable to metabolic disturbances.
  • Understanding the impact of GPA on cardiac function and protein expression is crucial for cardiovascular health research.

Purpose of the Study:

  • To investigate the effects of chronic GPA administration on protein profiling, energy metabolism, and right ventricular (RV) function in developing rat hearts.
  • To elucidate the role of the creatine kinase (CK) system in mediating these effects.
  • To assess the impact on cardiac growth and contractile performance.

Main Methods:

  • Chronic oral administration of GPA (1-1.5%) to rats during weaning and adolescence.
  • Measurement of cardiac tissue GPA accumulation, creatine, phosphocreatine, and ATP levels.
  • Analysis of creatine kinase (CK) isoenzyme distribution (Mi-CK, MB-CK).
  • Assessment of cardiac collagenous and non-collagenous protein content.
  • Evaluation of RV function using an isolated perfused heart model with pressure-volume analysis.

Main Results:

  • GPA accumulated in the myocardium, significantly decreasing total creatine, phosphocreatine, and ATP levels.
  • CK activity was unchanged, but Mi-CK proportion decreased and MB-CK increased.
  • Cardiac collagenous proteins increased, non-collagenous proteins decreased, and the collagen I/III ratio was reduced.
  • RV function was significantly impaired, with reduced systolic pressure, rate of pressure development, and cardiac output.
  • Blood plasma glucose, total lipids, and triglycerides remained unaffected.

Conclusions:

  • Chronic GPA administration profoundly impacts metabolic parameters, protein profiles, and contractile function in the developing heart.
  • The CK system is central to heart function and cardiac myocyte growth regulation.
  • GPA-induced metabolic disruption leads to impaired RV function and altered cardiac protein composition.

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