&quot；大鼠&quot；做强

霍普金斯大学的科学家们首次发现的蛋白质基因的缺失导致小鼠肌肉和男性超大已经找到了第二蛋白，卵泡抑素，其生产过剩在小鼠体内缺乏肌肉生长抑制素双打肌肉建设的影响。

硒金利的新研究结果，出现在本星期三PLoS ONE， show that while mice that lack the gene that makes myostatin have roughly twice the amount of body muscle as normal， mice without myostatin that also overproduce follistatin have about four times as much muscle as normal mice.

Lee， M.D.， Ph.D.， a professor of molecular biology and genetics， says that this added muscle increase could significantly boost research efforts to “beef up” livestock or promote muscle growth in patients with muscular dystrophy and other wasting diseases.

Specifically， Lee first discovered that follistatin was capable of blocking myostatin activity in muscle cells grown under lab conditions. When he gave it to normal mice， the rodents bulked up， just as would happen if the myostatin gene in these animals was turned off.

He then genetically engineered a mouse that both lacked myostatin and made extra follistatin. If follistatin was increasing muscle growth solely by blocking myostatin， then Lee surmised that follistatin would have no added effect in the absence of myostatin.

“To my surprise and delight， there was an additive effect，” said Lee， who notes these muscular mice averaged a 117 percent increase in muscle fiber size and a 73 percent increase in total muscle fibers compared to normal mice.

 “These findings show that the capacity for increasing muscle growth by targeting these pathways is much more extensive than we have appreciated，” adds Lee. “Now we’ll search for other players that cooperate with myostatin， so we can tap the full potential for enhancing muscle growth for clinical applications.” 

Lee adds that this issue is of particular significance， as most agents targeting this pathway， including one drug being currently tested in a muscular dystrophy clinical trial，  have been designed to block only myostatin and not other related proteins.

这项研究由美国国立卫生研究院和肌肉萎缩症协会由默克研究实验室资助的礼物。

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