Increased AMPK Activity Reduces Cancer-Related Loss of Muscle

Researchers here identify AMP-activated protein kinase (AMPK) as important in the loss of muscle that occurs in cancer patients, a wasting syndrome known as cachexia. They manage to reduce cachexia in mice. AMPK shows up in many considerations of metabolism and aging; to pick just a few, it can be used to extend life in flies, and appears to be involved in the mechanisms by which exercise improves health. Its role in these matters may be related to mitochondrial activity and cellular quality control, but like so many of these proteins it is involved in a large number of processes. An open question as a result of this research is the degree to which altered activity of AMPK might be involved in the loss of muscle mass and strength that occurs with aging, known as sarcopenia, or in other wasting conditions.

Healthy fat tissue is essential for extended survival in the event of tumor-induced wasting syndrome (cachexia). Cancer often results in weight loss due to unwanted metabolic complications. This so-called cancer cachexia is accompanied by a poor prognosis with regard to disease progression, quality of life, and mortality. After sepsis, cachexia is the most frequent cause of death in cancer patients. It is not entirely clear which biochemical mechanisms play a role. To date there have also not been any pharmacological possibilities for selectively influencing tumor-associated wasting syndrome.

Researchers have identified the AMP-activated protein kinase (AMPK) as the central enzyme in cancer cachexia. AMPK is normally responsible for protecting cells from energy deficiency. In the case of cancer cachexia, however, AMPK activity is inhibited due to the illness, resulting in a pointless waste of the body's own energy store. Selective AMPK reactivation was successfully carried out in tumor models. The therapeutic manipulation took place through a specific peptide which prevents the interaction between AMPK and the lipid droplet-associated protein Cidea, and which consequently can stop the increased fat breakdown (lipolysis) found in tumor diseases. "Our data suggest that the preservation of "healthy" adipose tissue can promote not only the quality of life, but also the response to treatment and the survival of cancer patients. The interaction between AMPK and Cidea can be taken as a starting point for developing new lipolysis inhibitors which could then prevent the breakdown of energy stores in the fat of tumor patients."



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