Quercetin regulates skeletal muscle fiber type switching <i>via</i> adiponectin signaling

Chen, Xiaoling; Liang, Dahui; Huang, Zhiqing; Jia, Gang; Zhao, Hua; Liu, Guangmang

doi:10.1039/d1fo00031d

Cited by 41 publications

(37 citation statements)

References 25 publications

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“…Interestingly, in this study, the addition of maca regulated skeletal muscle fiber type, especially MyHC-fast ( Figure 2 A). Previous studies showed that quercetin significantly increased the protein expression of MyHC-slow and significantly decreased MyHC-fast protein expression [ 26 ]. Since quercetin is also found in maca [ 27 ], we considered that maca may also have affected MyHC-slow, but no significant difference was detected in this study.…”

Section: Discussionmentioning

confidence: 99%

Effects of Maca on Muscle Hypertrophy in C2C12 Skeletal Muscle Cells

Dong

Yoshikawa

Sugimoto

et al. 2022

IJMS

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With aging, sarcopenia and the associated locomotor disorders, have become serious problems. The roots of maca contain active ingredients (triterpenes) that have a preventive effect on sarcopenia. However, the effect of maca on muscle hypertrophy has not yet been investigated. The aim of this study was to examine the effects and mechanism of maca on muscle hypertrophy by adding different concentrations of yellow maca (0.1 mg/mL and 0.2 mg/mL) to C2C12 skeletal muscle cell culture. Two days after differentiation, maca was added for two days of incubation. The muscle diameter, area, differentiation index, and multinucleation, were assessed by immunostaining, and the expression levels of the proteins related to muscle protein synthesis/degradation were examined by Western blotting. Compared with the control group, the muscle diameter and area of the myotubes in the maca groups were significantly increased, and the cell differentiation index and multinucleation were significantly higher in the maca groups. Phosphorylation of Akt and mTOR was elevated in the maca groups. Maca also promoted the phosphorylation of AMPK. These results suggest that maca may promote muscle hypertrophy, differentiation, and maturation, potentially via the muscle hypertrophic signaling pathways such as Akt and mTOR, while exploring other pathways are needed.

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Section: Discussionmentioning

confidence: 99%

Effects of Maca on Muscle Hypertrophy in C2C12 Skeletal Muscle Cells

Dong

Yoshikawa

Sugimoto

et al. 2022

IJMS

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“…This finding argues that innervation may play a dominant role in specifying fiber type by defining myofibrillar calcium oscillation and downstream signaling events ( Olson and Williams, 2000 ) required to match the metabolism of the cell with the contractile properties. On the other hand, shifting metabolism from oxidative to glycolytic phenotype, or vice versa, often leads to fiber type switching in the opposite direction ( Wen et al, 2020 ; Xu et al, 2020a , b ; Chen et al, 2021 ). For example, feeding mice with clenbuterol induces the de novo synthesis of IIX and IIB fibers in mouse soleus muscle, whose component are exclusively type I and IIA fiber ( Shi et al, 2007 ).…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies provide more evidence to support the notion that metabolites can drive muscle fiber switching through AMPK-PGC1α axis. For examples, quercetin, found in many fruits, vegetables and grains, can induce muscle fiber switching to a more oxidative phenotype through adiponectin-AMPK-PGC-1α pathway ( Chen et al, 2021 ). Dietary supplementation of arginine to mouse induces fast- to slow-twitch fiber type transition, accompanied by an upregulation of Sirt1/AMPK pathway ( Chen et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Driving an Oxidative Phenotype Protects Myh4 Null Mice From Myofiber Loss During Postnatal Growth

et al. 2022

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Postnatal muscle growth is accompanied by increases in fast fiber type compositions and hypertrophy, raising the possibility that a slow to fast transition may be partially requisite for increases in muscle mass. To test this hypothesis, we ablated the Myh4 gene, and thus myosin heavy chain IIB protein and corresponding fibers in mice, and examined its consequences on postnatal muscle growth. Wild-type and Myh4–/– mice had the same number of muscle fibers at 2 weeks postnatal. However, the gastrocnemius muscle lost up to 50% of its fibers between 2 and 4 weeks of age, though stabilizing thereafter. To compensate for the lack of functional IIB fibers, type I, IIA, and IIX(D) fibers increased in prevalence and size. To address whether slowing the slow-to-fast fiber transition process would rescue fiber loss in Myh4–/– mice, we stimulated the oxidative program in muscle of Myh4–/– mice either by overexpression of PGC-1α, a well-established model for fast-to-slow fiber transition, or by feeding mice AICAR, a potent AMP kinase agonist. Forcing an oxidative metabolism in muscle only partially protected the gastrocnemius muscle from loss of fibers in Myh4–/– mice. To explore whether traditional means of stimulating muscle hypertrophy could overcome the muscling deficits in postnatal Myh4–/– mice, myostatin null mice were bred with Myh4–/– mice, or Myh4–/– mice were fed the growth promotant clenbuterol. Interestingly, both genetic and pharmacological stimulations had little impact on mice lacking a functional Myh4 gene suggesting that the existing muscle fibers have maximized its capacity to enlarge to compensate for the lack of its neighboring IIB fibers. Curiously, however, cell signaling events responsible for IIB fiber formation remained intact in the tissue. These findings further show disrupting the slow-to-fast transition of muscle fibers compromises muscle growth postnatally and suggest that type IIB myosin heavy chain expression and its corresponding fiber type may be necessary for fiber maintenance, transition and hypertrophy in mice. The fact that forcing muscle metabolism toward a more oxidative phenotype can partially compensates for the lack of an intact Myh4 gene provides new avenues for attenuating the loss of fast-twitch fibers in aged or diseased muscles.

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“…Slow muscle fiber contains more mitochondria, has oxidative metabolism at a high level, and exhibits strong sustained contractile capacity. − Studies indicated that skeletal muscle fiber type switching from fast to slow fiber is important for the improvement of fatigue, alleviation of insulin resistance, and maintenance of body energy homeostasis. ,, Recently, increasing studies showed that natural products could induce skeletal muscle remodeling and increase the proportion of slow muscle fiber. − For instance, quercetin regulates skeletal muscle fiber type switching from glycolytic type II to oxidative type I; procyanidin B2 changes the composition proportion of myofiber types and increases slow muscle fiber gene expression; and lycopene promotes mitochondrial respiration, reduces glycolysis metabolism, and activates slow muscle fiber expression . In the present study, we found that naringin treatment could significantly increase oxidative enzymatic activity (SDH), up-regulate the expression of slow fiber-related genes TNNT1, PGC-1α, myoglobin, and MyHC I, and activate MyHC I protein expression, as well as decrease α-GPDH activity (α-GPDH is a hallmark of glycolytic metabolism, which is positively correlated with the proportion of IIb myofiber), down-regulate the expression of fast fiber-related genes TNNT3 and MyHC IIb expression, and reduce MyHC IIb protein expression.…”

Section: Discussionmentioning

confidence: 99%

Naringin Promotes Skeletal Muscle Fiber Remodeling by the AdipoR1-APPL1-AMPK Signaling Pathway

Zhang²,

Song

et al. 2021

J. Agric. Food Chem.

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Naringin, a natural flavonoid mainly found in citrus fruit, has been reported to exert a positive effect on improving skeletal muscle health. However, the effects and potential mechanisms of naringin on skeletal muscle fiber switching is still unclear. Here, we discovered that oral administration of naringin increased the low-speed running time, four-limb hanging time, body oxygen consumption in mice, enhanced aerobic enzyme activity, MyHC I expression, and slow-twitch fiber percentage in mice skeletal muscle. By contrast, naringin decreased α-GPDH enzyme activity, MyHC IIb expression, and fast-twitch fiber percentage. Moreover, naringin increased the concentration of serum adiponectin and activated the expression of AdipoR1, APPL1, AMPK, and PGC-1α. Furthermore, by the in vitro experiment and AdipoR1 knockdown, we found that inhibition of the AdipoR1 signaling pathway significantly reduced the effect of naringin on slow-twitch fiber-/fast-twitch fiber-related gene and protein expression. In conclusion, our results indicated that naringin could induce skeletal muscle fiber transition from fast twitch to slow twitch via the AdipoR1 signaling pathway. This study may provide new strategy for improving exercise endurance and slow muscle fiber deficiency-related diseases.

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Quercetin regulates skeletal muscle fiber type switching via adiponectin signaling

Abstract: This study aimed to investigate the role and underlying molecular mechanism of quercetin in regulating skeletal muscle fiber type transition. We found that dietary quercetin supplementation in mice significantly increased...

Cited by 41 publications

References 25 publications

Effects of Maca on Muscle Hypertrophy in C2C12 Skeletal Muscle Cells

Effects of Maca on Muscle Hypertrophy in C2C12 Skeletal Muscle Cells

Driving an Oxidative Phenotype Protects Myh4 Null Mice From Myofiber Loss During Postnatal Growth

Naringin Promotes Skeletal Muscle Fiber Remodeling by the AdipoR1-APPL1-AMPK Signaling Pathway

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