Overexpression of PGC-1αIncreases Fatty Acid Oxidative Capacity of Human Skeletal Muscle Cells | Zendy

Nataša Nikolić | Zendy; Magdalena Rhedin | Zendy; Arild C. Rustan | Zendy; L. H. Storlien | Zendy; G. Hege Thoresen | Zendy; Maria Strömstedt | Zendy

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Overexpression of PGC-1αIncreases Fatty Acid Oxidative Capacity of Human Skeletal Muscle Cells

Author(s) -

Nataša Nikolić,

Magdalena Rhedin,

Arild C. Rustan,

L. H. Storlien,

G. Hege Thoresen,

Maria Strömstedt

Publication year - 2011

Publication title -

biochemistry research international

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.631

H-Index - 36

eISSN - 2090-2255

pISSN - 2090-2247

DOI - 10.1155/2012/714074

Subject(s) - pdk4 , mitochondrial biogenesis , myogenesis , skeletal muscle , downregulation and upregulation , coactivator , microbiology and biotechnology , lipid metabolism , peroxisome proliferator activated receptor , beta oxidation , glycolysis , peroxisome , mitochondrion , biology , oxidative phosphorylation , endocrinology , medicine , biochemistry , receptor , metabolism , gene , transcription factor

We investigated the effects of PGC-1 α (peroxisome proliferator-activated receptor γ coactivator-1 α ) overexpression on the oxidative capacity of human skeletal muscle cells ex vivo . PGC-1 α overexpression increased the oxidation rate of palmitic acid and mRNA expression of genes regulating lipid metabolism, mitochondrial biogenesis, and function in human myotubes. Basal and insulin-stimulated deoxyglucose uptake were decreased, possibly due to upregulation of PDK4 mRNA. Expression of fast fiber-type gene marker (MHCIIa) was decreased. Compared to skeletal muscle in vivo , PGC-1 α overexpression increased expression of several genes, which were downregulated during the process of cell isolation and culturing. In conclusion, PGC-1 α overexpression increased oxidative capacity of cultured myotubes by improving lipid metabolism, increasing expression of genes involved in regulation of mitochondrial function and biogenesis, and decreasing expression of MHCIIa. These results suggest that therapies aimed at increasing PGC-1 α expression may have utility in treatment of obesity and obesity-related diseases.

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