Journal
NUTRIENTS
Volume 13, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/nu13020497
Keywords
auraptene; 7-geranyloxycoumarin; peroxisome proliferator-activated receptor-γ coactivator-1α mitochondria; skeletal muscle; muscle fiber; fruit; citrus fruit
Categories
Funding
- Council for Science, Technology, and Innovation (CSTI), Cross-ministerial Strategic Innovation Promotion Program (SIP) [14533567]
- Technologies for creating next-generation agriculture, forestry and fisheries (funding agency: Bio-oriented Technology Research Advancement Institution, NARO)
- KAKENHI of the Japanese Ministry of Education, Culture, Sports, Science and Technology (MEXT, Tokyo) [26282184]
- University of Shizuoka Grant for Scientific and Educational Research
- Grants-in-Aid for Scientific Research [26282184] Funding Source: KAKEN
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The study showed that Citrus hassaku extract powder can upregulate PGC-1 alpha expression in skeletal muscles, leading to increased mitochondrial biogenesis and transformation of muscle fibers into oxidative fibers. This suggests that CHEP may serve as a dietary supplement to prevent metabolic disorders.
Peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1 alpha) is expressed in skeletal muscles and regulates systemic metabolism. Thus, nutraceuticals targeting skeletal muscle PGC-1 alpha have attracted attention to modulate systemic metabolism. As auraptene contained in citrus fruits promotes lipid metabolism and improves mitochondrial respiration, it could increase mitochondrial function through PGC-1 alpha. Therefore, we hypothesized that PGC-1 alpha is activated by auraptene and investigated its effect using Citrus hassaku extract powder (CHEP) containing >80% of auraptene. C2C12 myotubes were incubated with vehicle or CHEP for 24 h; C57BL/6J mice were fed a control diet or a 0.25% (w/w) CHEP-containing diet for 5 weeks. PGC-1 alpha protein level and mitochondrial content increased following CHEP treatment in cultured myotubes and skeletal muscles. In addition, the number of oxidative fibers increased in CHEP-fed mice. These findings suggest that CHEP-mediated PGC-1 alpha upregulation induced mitochondrial biogenesis and fiber transformation to oxidative fibers. Furthermore, as CHEP increased the expression of the protein sirtuin 3 and of phosphorylated AMP-activated protein kinase (AMPK) and the transcriptional activity of PGC-1 alpha, these molecules might be involved in CHEP-induced effects in skeletal muscles. Collectively, our findings indicate that CHEP mediates PGC-1 alpha expression in skeletal muscles and may serve as a dietary supplement to prevent metabolic disorders.
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