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Protein Kinase (AMPK) and PGC-1α in Skeletal Muscle
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Permanent Link: http://ufdc.ufl.edu/UF00091523/00568
 Material Information
Title: Protein Kinase (AMPK) and PGC-1α in Skeletal Muscle
Series Title: Journal of Undergraduate Research
Physical Description: Serial
Language: English
Creator: Davila, Karla
Lira, Vitor A.
Criswell, David S. ( Mentor )
Publisher: University of Florida
Place of Publication: Gainesville, Fla.
Publication Date: 2009
 Notes
Abstract: Skeletal muscle is the major site of insulin-stimulated glucose uptake and oxidation processes which are controlled, in part, by activation of the cellular energy-sensor, AMP-activated protein kinase (AMPK). In addition, the transcription coactivator, peroxisome-proliferator activated receptor γ coactivator-1α (PGC-1α), has been considered to be a master regulator of cellular metabolism. Recently, nitric oxide (NO) was shown to be involved in mitochondrial biogenesis in skeletal muscle. Here we aim to find whether NO up-regulates PGC-1α mRNA expression in L6 myotubes and test whether the AMPK-dependent up-regulation of PGC-1α and mitochondrial genes are influenced by nitric oxide synthase (NOS) activity. METHODS: Rat L6 myotubes were differentiated by serum withdrawal to form confluent myotube cultures. Differentiated myotubes were exposed to various treatments and harvested for measurement of specific mRNAs via RT-real time PCR. RESULTS: Diethylenetriamine NONOate (DETA-NO; 50 μM) increased PGC-1α mRNA expression after 3 hr. This was a transient effect, returning to baseline at 6 hrs. Treatment with the AMPK activating compound, 5-aminoimidazole-4-carboxamide-1-ß -D-ribofuranoside (AICAR; 3 mM) increased phospho-to-total (α) AMPK ratio, and expression of mRNAs for PGC-1α, F1 ATP synthase, and citrate synthase, while co-treatment of myotubes with L-Nitroarginine methyl ester (L-NAME; 100μM), prevented these effects. CONCLUSIONS: NO is sufficient to induce PGC-1α mRNA, and NOS activity is required for AMPK activation, and induction of PGC-1α and mitochondrial gene expression.
 Record Information
Source Institution: University of Florida
Holding Location: University of Florida
Rights Management: All rights reserved by the source institution and holding location.
System ID: UF00091523:00568

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