The impact of a short‐term high‐fat diet on mitochondrial respiration, reactive oxygen species production, and dynamics in oxidative and glycolytic skeletal muscles of young rats

• Published in: Physiological reports 2018-02, Vol.6 (4), p.e13548-n/a
• Main Authors: Leduc‐Gaudet, Jean‐Philippe, Reynaud, Olivier, Chabot, François, Mercier, Jocelyne, Andrich, David E., St‐Pierre, David H., Gouspillou, Gilles
• Format: Article
• Language: English
• Subjects: Ageing and Degeneration; Animals; Carnitine; Cell Respiration; Diet, High-Fat; Electron transport chain; Endocrinology and Metabolism; Fatty acids; Fatty Acids - metabolism; Glycolysis; High fat diet; High‐fat feeding; lipid metabolism; Lipid Peroxidation; Male; Mitochondria; Mitochondria, Muscle - metabolism; Mitochondrial DNA; Mitochondrial Dynamics; mitochondrial fission; Muscle, Skeletal - metabolism; Musculoskeletal system; Original Research; Physiology; Protein turnover; Rats; Rats, Wistar; Reactive oxygen species; Reactive Oxygen Species - metabolism; Respiration; Rodents; Skeletal Muscle; Transcription; Uncoupling Protein 3 - metabolism
• ISSN: 2051-817X
• DOI: 10.14814/phy2.13548

Multiple aspects of mitochondrial function and dynamics remain poorly studied in the skeletal muscle of pediatric models in response to a short‐term high‐fat diet (HFD). This study investigated the impact of a short‐term HFD on mitochondrial function and dynamics in the oxidative soleus (SOL) and glycolytic extensor digitorum longus (EDL) muscles in young rats. Young male Wistar rats were submitted to either HFD or normal chow (NCD) diets for 14 days. Permeabilized myofibers from SOL and EDL were prepared to assess mitochondrial respiration and reactive oxygen species (ROS) production. The expression and content of protein involved in mitochondrial metabolism and dynamics (fusion/fission) were also quantified. While no effects of HFD was observed on mitochondrial respiration when classical complex I and II substrates were used, both SOL and EDL of rats submitted to a HFD displayed higher basal and ADP‐stimulated respiration rates when Malate + Palmitoyl‐L‐carnitine were used as substrates. HFD did not alter ROS production and markers of mitochondrial content. The expression of CPT1b was significantly increased in SOL and EDL of HFD rats. Although the expression of UCP3 was increased in SOL and EDL muscles from HFD rats, mitochondrial coupling efficiency was not altered. In SOL of HFD rats, the transcript levels of Mfn2 and Fis1 were significantly upregulated. The expression and content of proteins regulating mitochondrial dynamics was not modulated by HFD in the EDL. Finally, DRP1 protein content was increased by over fourfold in the SOL of HFD rats. Taken altogether, our findings show that exposing young animals to short‐term HFD results in an increased capacity of skeletal muscle mitochondria to oxidize fatty acids, without altering ROS production, coupling efficiency, and mitochondrial content. Our results also highlight that the impact of HFD on mitochondrial dynamics appears to be muscle specific. We show that short‐term high‐fat diet enhances mitochondrial capacity to oxidize fatty acids in both oxidative and glycolytic skeletal muscles without altering reactive oxygen species production in young rats. We also show that this enhanced mitochondrial capacity to oxidize fatty acids is not associated with an increase in markers of mitochondrial content, but with an upregulation of several key genes involved in lipid metabolism. Finally, our data indicate that a short‐term high‐fat diet increases DRP1 (a promitochondrial fusion protein) content specifical