Effects of Rhizome Extract of Dioscorea batatas and Its Active Compound, Allantoin, on the Regulation of Myoblast Differentiation and Mitochondrial Biogenesis in C2C12 Myotubes

Abstract

With the aging process, a loss of skeletal muscle mass and dysfunction related to metabolic syndrome is observed in older people. Yams are commonly use in functional foods and medications with various effects. The present study was conducted to investigate the effects of rhizome extract of Dioscorea batatas (Dioscoreae Rhizoma, Chinese yam) and its bioactive compound, allantoin, on myoblast differentiation and mitochondrial biogenesis in skeletal muscle cells. Yams were extracted in water and allantoin was analyzed by high performance liquid chromatography (HPLC). The expression of myosin heavy chain (MyHC) and mitochondrial biogenesis-regulating factors, peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), sirtuin-1 (Sirt-1), nuclear respiratory factor-1 (NRF-1) and transcription factor A, mitochondrial (TFAM), and the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) were determined in C2C12 myotubes by reverse transcriptase (RT)-polymerase chain reaction (RT-PCR) or western blot. The glucose levels and total ATP contents were measured by glucose consumption, glucose uptake and ATP assays, respectively. Treatment with yam extract (1 mg/mL) and allantoin (0.2 and 0.5 mM) significantly increased MyHC expression compared with non-treated myotubes. Yam extract and allantoin significantly increased the expression of PGC-1α, Sirt-1, NRF-1 and TFAM, as well as the phosphorylation of AMPK and ACC in C2C12 myotubes. Furthermore, yam extract and allantoin significantly increased glucose uptake levels and ATP contents. Finally, HPLC analysis revealed that the yam water extract contained 1.53% of allantoin. Yam extract and allantoin stimulated myoblast differentiation into myotubes and increased energy production through the upregulation of mitochondrial biogenesis regulators. These findings indicate that yam extract and allantoin can help to prevent skeletal muscle dysfunction through the stimulation of the energy metabolism.

Effect of Dietary Silk Peptide on Obesity, Hyperglycemia, and Skeletal Muscle Regeneration in High-Fat Diet-Fed Mice

“…The obesity-related loss of skeletal muscle, referred to as sarcopenia, is associated with the dysregulation of glucose metabolism and accelerated loss of muscle loss [69]. Therefore, a number of studies have focused on the mechanisms of this skeletal muscle dysfunction, as well as interrogating potential nutritional interventions, including the use of diets rich in protein, which could help retain muscle strength [70,71]. The present study has shown that SP increases the expression of genes involved in skeletal muscle differentiation in mice.…”

Constituents of Huberantha jenkinsii and Their Biological Activities

“…Neuroblastoma SH-SY5Y cells (5 × 10 4 cells/well) were seeded into each well. After 24 h incubation of the cells at 37 • C under 5% CO 2 , the sample was added to each well in four different concentrations (10,25,50, 100 µM), and the mixture was preincubated for 1 h. Then, the toxicity inducer 6-OHDA (6-hydroxy dopamine hydrobromide) was added, and the mixture was further incubated for 2 h. Ten microliters of resazurin was added to each well 1 h before the end of the incubation to obtain the final resazurin concentration of 0.01 mg/mL. Finally, the neuroprotective activity of each sample against 6-OHDA was determined by measuring the fluorescence intensity at 530 nm excitation and 590 nm emission wavelengths using a microplate reader.…”

The 5,7-Dimethoxyflavone Suppresses Sarcopenia by Regulating Protein Turnover and Mitochondria Biogenesis-Related Pathways

“…With an increasing age, the sarcopenia becomes regarded as a significant concern, which poses a substantial social and economic burden. In spite of great trials to pursue and develop agents and therapies, they remain unsatisfactory due to little convincing evidence and efficacy or accompanying side effects [6,7]. Currently, exercise training has been considered as a primary treatment for the sarcopenia or the muscle atrophy [6,7].…”

“…In spite of great trials to pursue and develop agents and therapies, they remain unsatisfactory due to little convincing evidence and efficacy or accompanying side effects [6,7]. Currently, exercise training has been considered as a primary treatment for the sarcopenia or the muscle atrophy [6,7]. However, there is a limitation to suggest exercise training as an intervention for sarcopenia because elderly people and sarcopenia patients are likely to be bed-ridden due to illness or frailty [1,2].…”