Authors: 
V. Pesce, F. Fracasso, P. Cassano, M. Calvani, L. Mosconi, P. Cantatore, M.N. Gadaleta
Category: 
Poster
Conference: 
Abstract: 

Decay of mitochondrial function is a major contributor to aging process, particularly for those post-mitotic tissues like skeletal muscle heavily dependent on oxidative metabolism (e.g. soleus). Aim of this study was to test if long-term ALCAR supplementation to aged rats was able to activate mitochondrial biogenesis in soleus muscle.

Young (6-month old) and old rats (28-month old) were used. Old rats were daily supplemented with ALCAR for 2 months. MtDNA content and transcript level of factors involved in mitochondrial biogenesis signalling pathway (PGC-1alpha, TFAM, TFB2) and of nuclear- and mitochondrial-coded genes (COX-IV, 16S rRNA, COX-I) were quantified by Real Time PCR. Protein level of PGC-1alpha and of two mitochondrial antioxidant enzymes, namely PrxIII and MnSOD, was also measured. Citrate synthase activity was determined as marker of mitochondrial mass content.

The obtained results revealed that ALCAR administration to old rats is able to prevent in soleus muscle the age-dependent decrease of mitochondrial decay. In particular, ALCAR treatment was able to upregulate the transcripts for master factors of mitochondrial biogenesis activating pathway, the mtDNA content and the mitochondrial mass. The protein level of PGC-1alpha and of the two mitochondrial enzymes PrxIII and MnSOD were also increased by ALCAR treatment.

ALCAR feeding could be, therefore, useful as dietary intervention in counteracting the age-related mammalian soleus muscle mitochondrial decay maintaining the oxidative fiber character of this muscle during aging.

Keywords (Optional): 
acetyl-l-carnitine
soleus muscle
mitochondrial biogenesis
aging