Not all the number of skeletal muscle fibers is determined prenatally

Li, Mingsen; Zhou, Xingyu; Chen, Yaosheng; Nie, Yaping; Huang, Haoyue; Hu, Chen; Mo, Delin

doi:10.1186/s12861-015-0091-8

Cited by 22 publications

(16 citation statements)

References 18 publications

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“…Imp2 has been proposed to contribute to myogenesis as a transcriptional target and proliferative effector of the DNA binding protein HMGA2; Imp2 can partially rescue the diminished proliferation of HMGA2-null myoblasts (24,25). Myogenesis in the mouse is largely completed prenatally, and the number of myofibers does not increase after postnatal day 7 (p7), although the number of nuclei/myofiber increases somewhat until p21 (26,27). In sedentary, uninjured mice, satellite cells, the adult muscle stem cells, are dispensable for the maintenance of muscle mass (28).…”

Section: Discussionmentioning

confidence: 99%

IMP2 Increases Mouse Skeletal Muscle Mass and Voluntary Activity by Enhancing Autocrine Insulin-Like Growth Factor 2 Production and Optimizing Muscle Metabolism

Regué

Flicker

et al. 2019

Molecular and Cellular Biology

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Insulin-like growth factor 2 (IGF2) mRNA binding protein 2 (IMP2) was selectively deleted from adult mouse muscle; two phenotypes were observed: decreased accrual of skeletal muscle mass after weaning and reduced wheel-running activity but normal forced treadmill performance. Reduced wheel running occurs when mice are fed a high-fat diet but is normalized when mice consume standard chow. The two phenotypes are due to altered output from different IMP2 client mRNAs. The reduced fiber size of IMP2-deficient muscle is attributable, in part, to diminished autocrine Igf2 production; basal tyrosine phosphorylation of the insulin and IGF1 receptors is diminished, and Akt1 activation is selectively reduced. Gsk3α is disinhibited, and S536-phosphorylated ε subunit of eukaryotic initiation factor 2B [eIF2Bε(S536)] is hyperphosphorylated. Protein synthesis is reduced despite unaltered mTOR complex 1 activity. The diet-dependent reduction in voluntary exercise is likely due to altered muscle metabolism, as contractile function is normal. IMP2-deficient muscle exhibits reduced fatty acid oxidation, due to a reduced abundance of mRNA of peroxisome proliferator-activated receptor α (PPARα), an IMP2 client, and PPARα protein. IMP2-deficient muscle fibers treated with a mitochondrial uncoupler to increase electron flux, as occurs with exercise, exhibit reduced oxygen consumption from fatty acids, with higher oxygen consumption from glucose. The greater dependence on muscle glucose metabolism during increased oxygen demand may promote central fatigue and thereby diminish voluntary activity.

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Section: Discussionmentioning

confidence: 99%

IMP2 Increases Mouse Skeletal Muscle Mass and Voluntary Activity by Enhancing Autocrine Insulin-Like Growth Factor 2 Production and Optimizing Muscle Metabolism

Regué

Flicker

et al. 2019

Molecular and Cellular Biology

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“…These data are unique in showing for the first time that growth of skeletal muscle is modulated by the combined actions of IGF1 and myostatin with each factor having a distinct role -myostatin regulates hyperplasia and IGF1 regulates hypertrophy of myofibres. It is likely that these two processes are temporally separated because the number of myofibres is largely fixed before birth (Rowe & Goldspink 1969, Timson & Dudenhoeffer 1990, although myogenesis can continue in the T. anterior and EDL muscles for up to a week postnatally (Li et al 2015). Therefore, the absence of myostatin throughout in utero development is likely to have increased the number of myofibres prenatally.…”

Section: Discussionmentioning

confidence: 99%

IGF1 stimulates greater muscle hypertrophy in the absence of myostatin in male mice

Hennebry

Oldham

Shavlakadze

et al. 2017

Journal of Endocrinology

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Insulin-like growth factors (IGFs) and myostatin have opposing roles in regulating the growth and size of skeletal muscle, with IGF1 stimulating, and myostatin inhibiting, growth. However, it remains unclear whether these proteins have mutually dependent, or independent, roles. To clarify this issue, we crossed myostatin null () mice with mice overexpressing in skeletal muscle () to generate six genotypes of male mice; wild type ( ), ,, , and Overexpression of increased the mass of mixed fibre type muscles (e.g. ) by 19% over , 33% over and 49% over ( < 0.001). By contrast, the mass of the gonadal fat pad was correspondingly reduced with the removal of and addition of Myostatin regulated the number, while IGF1 regulated the size of myofibres, and the deletion of and independently increased the proportion of fast type IIB myosin heavy chain isoforms in (up to 10% each, < 0.001). The abundance of AKT and rpS6 was increased in muscles of , while phosphorylation of AKT was increased in (, and). Our results demonstrate that a greater than additive effect is observed on the growth of skeletal muscle and in the reduction of body fat when myostatin is absent and IGF1 is in excess. Finally, we show that myostatin and IGF1 regulate skeletal muscle size, myofibre type and gonadal fat through distinct mechanisms that involve increasing the total abundance and phosphorylation status of AKT and rpS6.

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“…Skeletal muscle can withstand massive and sudden changes, both mechanically and bioenergetically, from rest to rapid contractile activity, because it has effective mechanisms for coping with ATP consumption and re-synthesis. While skeletal muscle is anatomically fixed at birth in mammals, postnatal muscle growth can undergo cellular changes, such as increases in length and girth, and some myofibers can experience changes in contractile activity and humoral factors in response to the nutrient availability [ 2 ]. The mammalian skeletal muscle can be classified across a spectrum, according to its contractile and metabolic properties, but it is broadly classified into two categories, namely, slow-twitch type I fibers and fast-twitch type II fibers.…”

Section: Skeletal Musclementioning

confidence: 99%

An aPPARent Functional Consequence in Skeletal Muscle Physiology via Peroxisome Proliferator-Activated Receptors

Phua

Wong

Liao

et al. 2018

IJMS

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Skeletal muscle comprises 30–40% of the total body mass and plays a central role in energy homeostasis in the body. The deregulation of energy homeostasis is a common underlying characteristic of metabolic syndrome. Over the past decades, peroxisome proliferator-activated receptors (PPARs) have been shown to play critical regulatory roles in skeletal muscle. The three family members of PPAR have overlapping roles that contribute to the myriad of processes in skeletal muscle. This review aims to provide an overview of the functions of different PPAR members in energy homeostasis as well as during skeletal muscle metabolic disorders, with a particular focus on human and relevant mouse model studies.

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Not all the number of skeletal muscle fibers is determined prenatally

Cited by 22 publications

References 18 publications

IMP2 Increases Mouse Skeletal Muscle Mass and Voluntary Activity by Enhancing Autocrine Insulin-Like Growth Factor 2 Production and Optimizing Muscle Metabolism

IMP2 Increases Mouse Skeletal Muscle Mass and Voluntary Activity by Enhancing Autocrine Insulin-Like Growth Factor 2 Production and Optimizing Muscle Metabolism

IGF1 stimulates greater muscle hypertrophy in the absence of myostatin in male mice

An aPPARent Functional Consequence in Skeletal Muscle Physiology via Peroxisome Proliferator-Activated Receptors

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