J Clin Endocrinol Metab. 2007 Nov 13.
Enhancement of Muscle Mitochondrial Function by Growth Hormone.
Short KR, Moller N, Bigelow ML, Coenen-Schimke J, Nair KS.
Endocrinology Research Unit, Mayo Clinic School of Medicine, Rochester, MN, USA.

Context: Though growth hormone (GH) promotes growth and protein anabolism, which are ATP-dependent processes, the GH effect on mitochondrial regulation remains to be determined. Objective: To determine the acute effect of GH on mitochondrial oxidative capacity in skeletal muscle of healthy subjects. Design: A randomized crossover design was used. Setting: Academic medical center. Participants: Nine healthy men and women completed the study. Intervention: GH (150microg/hr) or saline was infused for 14 h on separate days and muscle biopsies were obtained. Main Outcome Measures: Mitochondrial function, gene expression and protein metabolism. Results: The 4-fold increase in plasma GH caused elevations in plasma IGF-I, insulin, glucose, and free fatty acids, and a shift in fuel selection, with less carbohydrate (-69%) and leucine (-43%) oxidation and 29% more fat oxidation. Muscle mitochondrial ATP production rate and citrate synthase activity were increased 16-35% in response to GH. GH also resulted in higher abundance of muscle mRNAs encoding IGF-I, mitochondrial proteins from the nuclear (COX4) and mitochondrial (COX3) genomes, the nuclear-derived mitochondrial transcription factor A (TFAM), and glucose transporter 4. While GH increased whole body protein synthesis (non-oxidative disposal of leucine), no effect on synthesis rate of muscle mitochondrial proteins was observed. Conclusions: These results demonstrate that acute GH action promotes an increase in mitochondrial oxidative capacity and abundance of several mitochondrial genes. These events may occur through direct or indirect effects of GH on intracellular signaling pathways, but do not appear to involve a change in mitochondrial protein synthesis rate.

Categories: 2007, Energy metabolism, Mitochondria, Fatty acid metabolism, Fatty acid oxidation, Free fatty acids, Growth hormone physiology, Growth hormone treatment, IGF-1, Carbohydrate metabolism, Insulin, Amino acid oxidation, Citrate synthase