Chronic alcohol administration to rats induces mitochondrial biogenesis. Mitochondrial biogenesis could be a metabolic response to increase NADH re-oxidation and alcohol metabolism, beta oxidation of fatty acids and ATP generation, and/or the maintenance of intact mitochondrial DNA and adequate levels of mitochondrial transcripts. The mechanisms by which chronic alcohol induces mitochondrial biogenesis have not been fully explored. In this work, we explored the impact of a low fat diet and ethanol on mitochondrial biogenesis. Rats were fed an ethanol-containing diet intragastrically by total enteral nutrition for 21 days; control rats were administered isocaloric diets where carbohydrates substituted for EtOH calories. The diets provided 5% of calories as fat. Mitochondrial biogenesis was evaluated biochemically using the following markers: protein levels (evaluated by western blot) of peroxisome proliferator activated receptor gamma-coactivator 1 alpha and mitochondrial transcription factor A, citrate synthase activity, and activity of mitochondrial complexes II and IV. Citrate synthase and mitochondrial complex II and IV activities were increased by ethanol. Protein levels of peroxisome proliferator activated receptor gamma-coactivator 1 alpha and mitochondrial transcription factor A were not increased by ethanol. These results suggest that chronic ethanol, administered in a low fat diet model, increased mitochondrial biogenesis through a signaling pathway not dependent on peroxisome proliferator activated receptor gamma-coactivator 1 alpha.

Ethanol induces mitochondrial biogenesis in rats fed ethanol and a low-fat diet

251st National Meeting (2016)

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.