Miostatina (News- 2011~2012)

[Stokes]

Galera, pesquisei no fórum e soh encontrei artigos antigos sobre miostatina, coisa de 2010 pra traz, tenho uma coletânea sobre artigos, publicações, estudos e tudo mais sobre ela mais recente, porém nessa minha coletânea, algumas delas não tem data nem referência, então vou postar algumas... unica coisa é que não estão traduzidas, e to meio sem tempo, se quiserem traduzir e postar ou apenas comentar algo, irei ficar feliz, e ficarei mais feliz se postarem mais algum artigo que n tenho

uma coisa legal que eu achei e que n encontrei nos meus artigos eh que fizeram um estudo que comprovou que o dianabol diminue a miostatina e outra coisa é que parece que em doses reduzidas (3mg/kg-nao tenho certeza) não há efeitos no que diz respeito ao tamanho do coração...Fizeram tb testes em obesos morbitos em que tinham 2 grupos: os que fizeram redução de estomago e os que fizeram dieta e aerobico e esperou ambos os grupos perderem 30%de gordura, o grupo da redução de estomago teve queda da miostatina...

outra coisa: parece que um tempo atraz, fizeram estudos em humanos no brasil e teve um grupo de voluntários... alguem do forum foi volunatario e pode falar a respeito (n encontrei nada quando pesquisei no ferum)

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The natural aging process results in the physiological decline of multiple tissues and organ systems. Changes commonly occur with middle age and include decreased skeletal muscle mass, bone mineral density, cardiac output, insulin sensitivity and increased adiposity, all of which can contribute to the onset of sarcopenia, osteoporosis, heart failure or type 2 diabetes. Recent studies suggest that myostatin may influence many of these systems. We therefore sought to determine whether they are affected by aging, especially in "middle aged" mstn-/- mice (12 - 20 m.o.). Although body weights were similar in wild-type and mstn-/- mice, lean fat-free mass and skeletal muscles composed of predominantly type I, II and mixed fibers were significantly heavier in mstn-/- mice. These differences were accompanied by lower total adiposity, especially in female mice, white and brown fat pad weights and adipocyte size. Hearts were heavier in mstn-/- mice across a large age range (3-24 m.o.) and exhibited signs of dilated cardiomyopathy at rest, which include lower strain measurements compared to wild-type myocardium. However, mstn-/- mice responded better to isoproterenol stress tests with greater increases in fractional shortening and ejection fraction, differences that were again more apparent in females and which are consistent with physiological cardiac hypertrophy. Spleens and kidneys were also smaller, although histologically normal, in mstn-/- mice. These data together suggest that attenuating myostatin could potentially prevent or possibly treat pathological conditions that develop with age. Additional studies are nevertheless needed to definitively assess potential risks to cardiac function.

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Peroxisome Proliferator Activated Receptor β/δ induces myogenesis by modulating Myostatin activity

Background: PPARβ/δ has been implicated in muscle regeneration; however the signaling mechanism(s) is unclear.

Results: Activation of PPARβ/δ promoted Gasp-1 expression, blocked Myostatin activity and enhanced myogenesis.

Conclusion: Activation of PPARβ/δ led to inhibition of Myostatin activity and thus increased myogenesis.

Significance: PPARβ/δ agonists are novel Myostatin antagonists that have potential benefits towards improving postnatal muscle growth and repair.

Classically, PPARβ/δ function was thought to be restricted to enhancing adipocyte differentiation and development of adipose-like cells from other lineages. However, recent studies have revealed a critical role for PPARβ/δ during skeletal muscle growth and regeneration. Although PPARβ/δ has been implicated in regulating myogenesis, little is presently known about the role, and for that matter the mechanism(s) of action of PPARβ/δ in regulating postnatal myogenesis. Here we report for the first time, using a PPARβ/δ-specific ligand (L165041) and the PPARβ/δ-null mouse model, that PPARβ/δ enhances postnatal myogenesis through increasing both myoblast proliferation and differentiation. In addition, we have identified Gasp-1 (Growth and differentiation factor associated serum protein-1) as a novel downstream target of PPARβ/δ in skeletal muscle. In agreement, reduced Gasp-1 expression was detected in PPARβ/δ-null mice muscle tissue. We further report that a highly conserved PPAR responsive element (PPRE) within the 1.5kb proximal Gasp-1 promoter region is critical for PPARβ/δ regulation of Gasp-1. Gasp-1 has been reported to bind to and inhibit the activity of Myostatin; consistent with this, we find enhanced secretion of Gasp-1, increased Gasp-1 Myostatin interaction and significantly reduced Myostatin activity upon L165041-mediated activation of PPARβ/δ. Moreover, we have analyzed the ability of hGASP-1 to regulate myogenesis, independent of PPARβ/δ activation. Results reveal that hGASP-1 protein treatment enhances myoblast proliferation and differentiation, whereas silencing of hGASP-1 results in defective myogenesis. Taken together these data reveal that PPARβ/δ is a positive regulator of skeletal muscle myogenesis, which functions through negatively modulating Myostatin activity via a mechanism involving Gasp-1.

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Myostatin, Muscles and Bodyfat

By: Jerry Brainium

Myostatin is a protein discovered by researchers at Johns Hopkins University in 1997. The word myostatin means 'muscle stopper,' an accurate description of what it does in the body. Scientists aren't sure how myostatin works, but the leading theory is that it inhibits the involvement of satellite cells, or immature muscle cells, in muscle growth. That's the opposite of what several anabolic hormones, particularly insulinlike growth factor 1 (IGF-1), do.

Animals born without the gene that codes for myostatin have two primary characteristics: They have much larger muscles than usual, and they have less bodyfat than usual. Other than that, they appear normal, with no obvious physical problems.

Myostatin is a topic of enormous interest to bodybuilders, since, theoretically, if you can somehow block its effects, your muscles will grow like crazy. As noted previously in this space, weight training is an effective myostatin blocker, which accounts for some of the growth that comes from regular training. In animals, blocking myostatin activity or manipulating their genes so that they don't produce myostatin yields not only increased muscular growth but also a dramatic reduction in bodyfat. The theory is that the lack of myostatin produces a repartitioning effect, promoting muscle growth at the expense of bodyfat. In short, bodyfat is used as a source of energy to support muscle growth.

A new study partially illuminates the relationship between myostatin and bodyfat levels.1 It involved six morbidly obese (a medical euphemism for 'very fat') subjects who underwent surgery to shorten their stomachs. That limits the amount of food they can eat without feeling full. The surgery is considered extreme and is a last resort for people with dangerously high bodyfat levels, people who, for some reason or other, will not or cannot diet and exercise. The side effects of the surgery can include death'but that's another story.

As a result of the surgery, the patients lost 38.9 percent of their bodyweight. The researchers measured their myostatin levels before and after the weight loss and found a clear and significant decline in myostatin after the weight loss, which consisted mostly of bodyfat. The scientists suggest that the drop in myostatin was the body's way of preventing the loss of vital lean mass under rapid and extreme fat-loss conditions. The drop in myostatin apparently had the effect of preventing muscle loss and may have also helped the body actually reduce the size of fat cells, as it does in animals.

Even though bodybuilders don't resort to stomach stapling as a fat-loss technique, the study has two implications for them. As you lose fat, myostatin levels will likely decline, helping you preserve muscle during a diet. The addition of a weight-training routine will no doubt amplify the effect. The other implication is that having excess bodyfat probably increases myostatin, making it harder to build muscle. That's been the case in a few studies of obese people who begin weight-training programs. They often start with considerable amounts of lean mass under the fat, but, compared to their leaner peers, they seen to have trouble adding muscle mass. Perhaps the higher levels of myostatin preclude significant muscle gains.

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Créditos:

https://joe.endocrino...1-0455.abstract

https://www.ironmanma...rticle&go2=1090

Editado Abril 30, 2012 às 01:46 por Stokes

[brunoyf]

Aguardando ansiosamente alguem traduzir...

[Stokes]

le em ingles pow... terça btf que tenho tempo para traduzir algum texto