A Ketogenic Diet Increases Succinic Dehydrogenase Activity in Aging Cardiomyocytes
- 15 August 2009
- journal article
- Published by Wiley in Annals of the New York Academy of Sciences
- Vol. 1171 (1), 377-384
- https://doi.org/10.1111/j.1749-6632.2009.04704.x
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.Keywords
This publication has 39 references indexed in Scilit:
- The role of the electron transport gene SDHC on lifespan and cancerExperimental Gerontology, 2006
- Caspase-dependent and -independent cell death induced by 3-nitropropionic acid in rat cortical neuronsJournal of Cellular Biochemistry, 2005
- Efficacy of levo carnitine and alpha lipoic acid in ameliorating the decline in mitochondrial enzymes during agingClinical Nutrition, 2005
- Facilitated glucose transporter protein type 1 (GLUT1) deficiency syndrome: impaired glucose transport into brain – a reviewEuropean Journal of Pediatrics, 2002
- Mitochondrial Decay in the Aging Rat HeartAnnals of the New York Academy of Sciences, 2002
- β-Hydroxybutyrate, a Cerebral Function Improving Agent, Protects Rat Brain Against Ischemic Damage Caused by Permanent and Transient Focal Cerebral IschemiaThe Japanese Journal of Pharmacology, 2002
- Ketone Bodies, Potential Therapeutic UsesIUBMB Life, 2001
- Intracellular Calcium, DNase Activity and Myocyte Apoptosis in Aging Fischer 344 RatsJournal of Molecular and Cellular Cardiology, 1998
- The potential for endogenous myocardial antioxidants to protect the mycocardium against ischaemia-reperfusion injury: Refreshing the parts exogenous antioxidants cannot reach?Journal of Molecular and Cellular Cardiology, 1995
- Comparison between developmental and senescent changes in enzyme activities linked to energy metabolism in rat heartMechanisms of Ageing and Development, 1981