Skeletal muscle as an endocrine organ: PGC-1α, myokines and exercise

Schnyder, Svenia; Handschin, Christoph

doi:10.1016/j.bone.2015.02.008

Cited by 343 publications

(272 citation statements)

References 191 publications

(220 reference statements)

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“…TH-induced mitochondrial biogenesis occurs through stimulation of the expression of intermediate factors, especially the transcription factor peroxisome proliferatoractivated receptor coactivator 1α (PGC1A), which is a key regulator of mitochondrial biogenesis in SM (Schnyder & Handschin 2015). T 3 positively regulated PGC1A by THR directly on the gene promoter (Fig.…”

Section: Thyroid Hormone Affects Skeletal Muscle Metabolismmentioning

confidence: 99%

Role of thyroid hormone in skeletal muscle physiology

Bloise

Cordeiro

Ortiga-Carvalho

2018

Journal of Endocrinology

146

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Thyroid hormones (TH) are crucial for development, growth, differentiation, metabolism and thermogenesis. Skeletal muscle (SM) contractile function, myogenesis and bioenergetic metabolism are influenced by TH. These effects depend on the presence of the TH transporters MCT8 and MCT10 in the plasma membrane, the expression of TH receptors (THRA or THRB) and hormone availability, which is determined either by the activation of thyroxine (T 4 ) into triiodothyronine (T 3 ) by type 2 iodothyronine deiodinases (D2) or by the inactivation of T 4 into reverse T 3 by deiodinases type 3 (D3). SM relaxation and contraction rates depend on T 3 regulation of myosin expression and energy supplied by substrate oxidation in the mitochondria. The balance between D2 and D3 expression determines TH intracellular levels and thus influences the proliferation and differentiation of satellite cells, indicating an important role of TH in muscle repair and myogenesis. During critical illness, changes in TH levels and in THR and deiodinase expression negatively affect SM function and repair. This review will discuss the influence of TH action on SM contraction, bioenergetics metabolism, myogenesis and repair in health and illness conditions.

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Section: Thyroid Hormone Affects Skeletal Muscle Metabolismmentioning

confidence: 99%

Role of thyroid hormone in skeletal muscle physiology

Bloise

Cordeiro

Ortiga-Carvalho

2018

Journal of Endocrinology

146

View full text Add to dashboard Cite

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“…In addition, metabolic changes in a peripheral organ can affect the physiology of other peripheral organs (2,3). The skeletal muscle system, which is newly recognized as playing endocrine-related roles, produces myokines after exercise to target other metabolic organs (liver, adipose tissue, pancreas, gut, and bone) and modulates systemic energy homeostasis (4).…”

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confidence: 99%

Activin signaling mediates muscle-to-adipose communication in a mitochondria dysfunction-associated obesity model

Song

Owusu-Ansah

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Mitochondrial dysfunction has been associated with obesity and metabolic disorders. However, whether mitochondrial perturbation in a single tissue influences mitochondrial function and metabolic status of another distal tissue remains largely unknown. We analyzed the nonautonomous role of muscular mitochondrial dysfunction in Drosophila. Surprisingly, impaired muscle mitochondrial function via complex I perturbation results in simultaneous mitochondrial dysfunction in the fat body (the fly adipose tissue) and subsequent triglyceride accumulation, the major characteristic of obesity. RNA-sequencing (RNA-seq) analysis, in the context of muscle mitochondrial dysfunction, revealed that target genes of the TGF-β signaling pathway were induced in the fat body. Strikingly, expression of the TGF-β family ligand, Activin-β (Actβ), was dramatically increased in the muscles by NF-κB/Relish (Rel) signaling in response to mitochondrial perturbation, and decreasing Actβ expression in mitochondrial-perturbed muscles rescued both the fat body mitochondrial dysfunction and obesity phenotypes. Thus, perturbation of muscle mitochondrial activity regulates mitochondrial function in the fat body nonautonomously via modulation of Activin signaling.mitochondrial synchrony | Activin-β | complex I perturbation | NF-κB/Relish | lipid metabolism I ndividual organs in a multicellular organism, besides performing their respective roles, must communicate with other organs to maintain systemic homeostasis. The central nervous system (CNS) in particular integrates information regarding the status of peripheral metabolic processes via hormonal signaling and directs energy homeostasis and feeding behavior (1). In addition, metabolic changes in a peripheral organ can affect the physiology of other peripheral organs (2, 3). The skeletal muscle system, which is newly recognized as playing endocrine-related roles, produces myokines after exercise to target other metabolic organs (liver, adipose tissue, pancreas, gut, and bone) and modulates systemic energy homeostasis (4).Mitochondria are semiautonomous organelles that integrate multiple physiological signals. Growing evidence indicates that mitochondrial alterations in one organ leads to abnormalities in biological processes in distal organs through hormonal signaling (5, 6). In addition to exercise, which induces mitochondrial activity and improves muscle performance, mitochondrial perturbationassociated muscle injury is also sufficient to modulate functions of other organs and change systemic outcomes via myokine production. For example, in mammals, mitochondrial dysfunction due to disruption of autophagic function in skeletal muscles results in elevated production of muscular FGF21 that triggers browning of white adipose tissue and increases lipid mobilization (7). Further, in Drosophila, mild mitochondrial distress in adult muscles delays aging via an increase of muscular ImpL2 production and remote suppression of insulin signaling in the fat body and brain (8). Despite these examples, molecula...

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“…In the brain, FNDC5/irisin expression was demonstrated to increase the expression of brain-derived neurogenic growth factor BDNF. 36 BDNF synthesis and secretion in the hippocampus promotes brain development including neuronal cell survival, differentiation, migration, dendritic arborization, synaptogenesis and plasticity 9 leading to regulation of hippocampal learning and memory. 37 One goal of the present study was to evaluate the effect of short-term exercise on cognitive functions in obese and normal weight subject.…”

Section: 35mentioning

confidence: 99%

Physical Exercise Induces Irisin Levels Associated With Improved Cognitive Functions and Glucose Tolerance in Obese and Normal Weight Egyptian Subjects: A 3-Month Interventional Study.

Shehta¹,

Elsaid²,

Raafat³

et al. 2017

IJAR

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Introduction:Cognitive impairment and glucose intolerance are prevalent in obese subjects. Irisin, a recently identified modifier of cognitive functions and glucose metabolism, was reported to be induced by physical exercise. We examined the association of exerciseinduced irisin levels with improved cognitive functions and glucose metabolism in both obese and normal weight subjects. Subjects and Methods: 120 subjects, both males and females, comprised of 60 obese and 60 normal-weight subjects were undergone supervised active aerobic exercises for 3-months. Irisin levels, cognitive functions, fasting blood glucose, insulin, homeostatic model assessment of insulin resistance index (HOMA-IR) were assessed at the initiation and termination of the study. Results: Obese subjects demonstrated lower irisin levels, impaired cognitive functions and higher insulin as well as HOMA-IR levels compared to the normal weight group. Physical exercise induced significant upregulation of irisin levels together with improvement of cognitive functions and significant reduction of insulin and HOMA-IR levels in both groups. Exercise-induced irisin levels demonstrated significant positive correlations with improved cognitive functions and significant negative correlation with insulin level and HOMA-IR. Conclusion: Physical exercise improves cognitive functions and glucose metabolism. Our results suggest that irisin could be an important molecular mediator and therapeutic target for improving cognitive functions and glucose metabolism.

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Skeletal muscle as an endocrine organ: PGC-1α, myokines and exercise

Cited by 343 publications

References 191 publications

Role of thyroid hormone in skeletal muscle physiology

Role of thyroid hormone in skeletal muscle physiology

Activin signaling mediates muscle-to-adipose communication in a mitochondria dysfunction-associated obesity model

Physical Exercise Induces Irisin Levels Associated With Improved Cognitive Functions and Glucose Tolerance in Obese and Normal Weight Egyptian Subjects: A 3-Month Interventional Study.

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