BernheimV1, Hal, Checkpoint, bibRecord, 000073

Caracterisation of signaling pathways controled by androgens in mouse striated muscle

Identifieur interne : 000073 ( Hal/Checkpoint ); précédent : 000072; suivant : 000074

Caracterisation of signaling pathways controled by androgens in mouse striated muscle

Auteurs : Me Lanie Schuh [France]

Source :

RBID : Hal:tel-01236155

Descripteurs français

mix :
- Anabolisme, Androgènes, Autophagie, Catabolisme, Cellules satellites, Force, Muscle squelettique, Myofibres, Récepteur des androgènes.
Wicri :
- topic : Glucose.

English descriptors

mix :
- Anabolism, Androgen, Androgen receptor, Autophagy, Catabolism, Glucose, Myofibers, Polyamines, Satellite cells, Skeletal muscle, Strength.

Abstract

Muscles generate strength and movement, and have important metabolic functions. The aim of my work was to characterize the role and mechanisms of action of androgen receptor in skeletal muscle. We show that ablation of the androgen receptor in skeletal muscle myofibers does not affect muscle mass as both anabolic (IGF1) and catabolic pathways (myostatin) are deregulated. However, the absence of this receptor in myofibers decreases muscle hypertrophy induced by mechanical overload and limits glucocorticoids-induced muscle atrophy. Its ablation also increases autophagy, leading to sacromeres destructuration, resulting in decreased muscle strength. Moreover, its deletion reduced the rate of glucose absorption during a glucidic overload. Thus, myofibres androgen receptor regulates muscle mass and strength, as well as glucose import.

Url:

https://tel.archives-ouvertes.fr/tel-01236155

Links toward previous steps (curation, corpus...)

to stream Hal, to step Corpus: 000022
to stream Hal, to step Curation: 000022

Links to Exploration step

Hal:tel-01236155

Le document en format XML

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<front><div type="abstract" xml:lang="en">Muscles generate strength and movement, and have important metabolic functions. The aim of my work was to characterize the role and mechanisms of action of androgen receptor in skeletal muscle. We show that ablation of the androgen receptor in skeletal muscle myofibers does not affect muscle mass as both anabolic (IGF1) and catabolic pathways (myostatin) are deregulated. However, the absence of this receptor in myofibers decreases muscle hypertrophy induced by mechanical overload and limits glucocorticoids-induced muscle atrophy. Its ablation also increases autophagy, leading to sacromeres destructuration, resulting in decreased muscle strength. Moreover, its deletion reduced the rate of glucose absorption during a glucidic overload. Thus, myofibres androgen receptor regulates muscle mass and strength, as well as glucose import.</div>
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            <abstract xml:lang="en">Muscles generate strength and movement, and have important metabolic functions. The aim of my work was to characterize the role and mechanisms of action of androgen receptor in skeletal muscle. We show that ablation of the androgen receptor in skeletal muscle myofibers does not affect muscle mass as both anabolic (IGF1) and catabolic pathways (myostatin) are deregulated. However, the absence of this receptor in myofibers decreases muscle hypertrophy induced by mechanical overload and limits glucocorticoids-induced muscle atrophy. Its ablation also increases autophagy, leading to sacromeres destructuration, resulting in decreased muscle strength. Moreover, its deletion reduced the rate of glucose absorption during a glucidic overload. Thus, myofibres androgen receptor regulates muscle mass and strength, as well as glucose import.</abstract>
            <abstract xml:lang="fr">Les muscles permettent de générer force et mouvements et ont des fonctions métaboliques importantes. Mon travail a consisté à caractériser le rôle et les mécanismes d’actions des androgènes dans le muscle strié. Nous avons montré que l’ablation du récepteur des androgènes dans les myofibres n’affecte pas la masse musculaire car à la fois les voies anaboliques (IGF1) et cataboliques (myostatine) sont dérégulées. Cependant, l’absence du récepteur dans les myofibres diminue l’hypertrophie musculaire induite par une surcharge mécanique et limite l’atrophie induite par les glucocorticoïdes. Son ablation augmente également l’autophagie, entrainant une déstructuration des sarcomères, conduisant à une diminution de la force musculaire. De plus, sa délétion diminue la vitesse d’absorption du glucose lors d’une surcharge glucidique. Le récepteur des androgènes dans les myofibres régule donc la masse et la force musculaire, ainsi que l’import du glucose.</abstract>
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Caracterisation of signaling pathways controled by androgens in mouse striated muscle

Caracterisation of signaling pathways controled by androgens in mouse striated muscle

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri