Secret of Insulin-Like Growth Factor Revealed.

Bodybuilders take insulin-like growth factors (IGFs) to promote muscle-building, and scientists have studied their effects on muscle and their role in the growth and spread of cancer, but experts had been unable to uncover the secret of how IGFs work on muscle cells, until now.

Insulin-like growth factors are a type of hormone that is secreted from many different cells. The two main IGFs are IGF-I and IGF-II, and both resemble insulin in structure. IGFs work by attaching themselves to receptors on target cells. This triggers a series of reactions that direct the cell to do something.

When muscle is being formed, the binding of IGF to a receptor can trigger one of two responses from the myoblasts, which are immature cells that develop into muscle tissue. One, the cells divide; or two, the cells become specialized. Once a muscle cell takes one course of action, it cannot take another action at a later time. Experts have long wondered how stimulation of the same receptor by the same hormone can trigger two very different responses, and now Cumming Duan, a molecular biologist at the University of Michigan, believes he and his team have found the answer, and the answer is oxygen.

It appears that the ability of myoblasts to respond is determined by the amount of oxygen that is available. When there is an adequate amount of oxygen, IGF promotes differentiation of muscle cells, but when oxygen levels are below normal, IGF promotes muscle cell division. When oxygen is low, a factor called the HIF-1 complex reprograms the steps that ultimately control the cell’s response.

These findings may be useful in several areas, including muscle loss (atrophy) as people grow older. Duan notes that “If we can find a way to affect IGF signaling, we may be able to stop or reverse the loss.” The researchers also believe their findings could result in new treatments for muscle-wasting diseases, shed light on the role of IGFs in cancer, and possibly lead to new ways to treat cancer.

SOURCE:
University of Michigan news release, Mar. 15, 2010

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