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A Ketogenic Diet Increases Succinic Dehydrogenase Activity in Aging Cardiomyocytes
Author(s) -
Balietti Marta,
Fattoretti Patrizia,
Giorgetti Belinda,
Casoli Tiziana,
Di Stefano Giuseppina,
Solazzi Moreno,
Platano Daniela,
Aicardi Giorgio,
BertoniFreddari Carlo
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.04704.x
Subject(s) - medicine , endocrinology , ketogenic diet , ketone bodies , succinate dehydrogenase , mitochondrion , reactive oxygen species , chemistry , glycolysis , metabolism , biology , biochemistry , neuroscience , epilepsy
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.