Mitochondrial biogenesis is defined as the growth and division of pre-existing mitochondria. Mitochondrial biogenesis is triggered by environmental stresses that activate a transcriptional program that upregulates the expression of mitochondrial biogenesis genes. These genes include co-activators such as peroxisome proliferator-activated receptor gamma-coactivator- 1 alpha (PGC1a, the master regulator of mitochondrial biogenesis) and DNA-binding transcription factors such as mitochondrial transcription factor A (TFAM). Ethanol administration to experimental animals can affect hepatic mitochondrial biogenesis, inducing mitochondrial depletion or proliferation, depending on experimental protocols. Key variables that determine the effect of ethanol on mitochondrial biogenesis are the concentration of ethanol, duration of exposure, ways of administration (oral of intragastric), and animal species. In this work we explored the effect of chronic (4 weeks) oral ethanol administration (at 36% of total calories) on hepatic mitochondrial biogenesis in mice. The expression of PGC1a and TFAM was evaluated at the protein level by western blotting, against beta actin as a loading control. Quantification of the bands by densitometry showed that the PGC1a and TFAM content did not change in mice exposed to oral ethanol for 4 weeks (with respect to the controls), in contrast with published results showing increased hepatic PGC1a and TFAM expression in mice exposed to ethanol intragastrically for 4 weeks. These results suggest that the effect of ethanol on hepatic mitochondrial biogenesis depend critically on the administration protocol.

Effect of oral chronic ethanol administration on hepatic mitochondrial biogenesis in mice

249th National Meeting (2015)

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