A ketogenic diet increases succinic dehydrogenase activity in aging cardiomyocytes: Potential protective role against apoptosis-induced heart failure

Marta Balietti, Patrizia Fattoretti, Belinda Giorgetti, Tiziana Casoli, Giuseppina Di Stefano, Moreno Solazzi, Daniela Platano, Giorgio Aicardi, Carlo Bertoni-Freddari

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Abstract

Impairment of energy metabolism and an increase of reactive oxygen species (ROS) production seem to play a major role in age-related apoptotic loss of cardiomyocytes. Succinic dehydrogenase (SDH) is an important marker of the mitochondrial capability to provide an adequate amount of ATP. Moreover, because of its unique redox properties, SDH activity contributes to maintain the reduced state of the ubiquinone pool. Recent reports have shown that ketone body intake improves cardiac metabolic efficiency and exerts a cardioprotective antioxidant action, we therefore performed a cytochemical investigation of SDH activity in cardiomyocytes of late-adult (19-month-old) rats fed for 8 weeks with a medium-chain triglycerides ketogenic diet (MCT-KD). Young, age-matched and old animals fed with a standard chow were used as controls. The overall area of the precipitates (PA) from SDH activity and the area of the SDH-positive mitochondria (MA) were measured. The percent ratios PA/MA and MA/total myocardial tissue area (MA/TA) were the parameters taken into account. We found that PA/MA was significantly higher in young control rats and in MCT-KD-fed rats versus late-adult and old control rats and in young control versus MCT-KD-fed rats. MA/TA of MCT-KD-fed rats was significantly higher versus age-matched and old control rats and tended to be higher versus young control rats; this parameter was significantly higher in young versus old control rats. Thus, MCT-KD intake partially recovers age-related decrease of SDH activity and increases the myocardial area occupied by metabolically active mitochondria. These effects might counteract metabolic alterations leading to apoptosis-induced myocardial atrophy and failure during aging.

Original languageEnglish
Title of host publicationAnnals of the New York Academy of Sciences
Pages377-384
Number of pages8
Volume1171
DOIs
Publication statusPublished - Aug 2009

Publication series

NameAnnals of the New York Academy of Sciences
Volume1171
ISSN (Print)00778923
ISSN (Electronic)17496632

Keywords

  • Aging
  • Apoptosis
  • Atrophy
  • Heart
  • Ketogenic diet
  • Mitochondria
  • Succinic dehydrogenase

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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