In a new study involving mice with implanted tumors, another catabolic pathway was found to be the predominant cause of cachexia and associated muscle-wasting. This pathway involves the activin type-2 receptor (AT2R). Activin is known to be involved in the release of myostatin, a protein that prevents muscle hypertrophy and promotes muscle catabolism or breakdown. In the mouse study, researchers injected the mice with a soluble version of AT2R. Previous studies have shown when this substance was supplied to mice, it dramatically blunted the activity of myostatin, resulting in significant growth of muscle mass. Providing AT2R to mice with tumors extended their lives by several weeks, despite having no effect on the tumors themselves or on bodyfat losses. In fact, the cancer-stricken mice even showed a gain in muscle mass.Based on this finding, the study authors suggest that blocking the activity of AT2R may extend the life of those afflicated with any type of disease that features a massive loss of muscle.
Besides preserving skeletal muscle mass, the soluble injectable version of AT2R also reversed the loss of cardiac muscle. Elevated levels of myostatin have been previously implicated in causing heart failure, which makes sense since the heart is a muscle, and myostatin helps to degrade muscle.
From a bodybuilding and exercise standpoint, myostatin has held a particular fascination because of its potent effects of promoting muscle mass in animals. It not only produces larger muscles, but also promotes a loss of bodyfat. On the negative side, myostatin is required for connective tissue repair, and blocking it could result in increased tendon and ligament injuries. Various supplements have been offered that are touted to block myostatin. These included a seaweed-based compound that worked well in test-tube studies, but did nothing for intact human bodies. A more recent version is derived from eggs, known as follistatin. This version is no doubt based on animal studies showing that injected follistatin does indeed effectively block myostatin,. But there is as yet no convincing evidence that an oral supplement would duplicate the effect. This is particularly true because follistatin is a protein, and would undergo the typical digestive effects of all orally ingested proteins, which of course would inactivate it.
Zhou X, et al. Reversal of cancer cachexia ands muscle wasting by ActR2-B antagonism leads to prolonged survival. Cell 2010;142:531-43.
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