Can cancer cachexia be prevented/treated?

[...]muscles from the animals treated with the histone deacetylase inhibitor trichostatin A displayed an increased production of follistatin and an increased expression of markers of regeneration after muscle injury, suggesting that follistatin has fusigenic effects exerted by the deacetylase inhibi...

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Published in:Nutrition (Burbank, Los Angeles County, Calif.) Los Angeles County, Calif.), 2012-09, Vol.28 (9), p.844-848
Main Author: Das, Undurti N., M.D., F.A.M.S
Format: Article
Language:English
Subjects:
Body Mass Index
Cachexia - metabolism
Cancer
Diet
Female
Gastroenterology and Hepatology
Humans
Insulin resistance
Intra-Abdominal Fat - metabolism
Male
Metabolism
Muscular system
Neoplasms - complications
Proteins
Subcutaneous Fat - metabolism
Weight control
Weight Loss - physiology
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Summary:[...]muscles from the animals treated with the histone deacetylase inhibitor trichostatin A displayed an increased production of follistatin and an increased expression of markers of regeneration after muscle injury, suggesting that follistatin has fusigenic effects exerted by the deacetylase inhibitors on skeletal muscles [18]. [...]it appears that the modulation of myostatin and follistatin expression and action could form a rational approach to manipulate skeletal myogenesis, promote muscle regeneration and preadipocyte differentiation, and regulate the lipid metabolism of mature adipocytes that may aid in the prevention and treatment of cancer cachexia and cachexia in other conditions.\n Glucose homeostasis studies using hyperinsulinemic-euglycemic clamping and radioisotopic tracer kinetics showed that RAP-031 increased the glucose infusion and disposal rates by 119% and 45%, respectively, and suppressed hepatic glucose production by 66% [21]. In view of these evidences, it would have been interesting if Agustsson et al. had studied the expression of myostatin in the skeletal muscle and adipose tissue in their study subjects and the levels of myostatin in their plasma and probably study the myostatin gene polymorphism in their future studies. Because myostatin is an extracellular cytokine mostly expressed in the skeletal muscles, is known to play a crucial role in the negative regulation of muscle mass, and is a potent negative regulator of brown adipogenic differentiation by the modulation of Smad3-induced β-catenin stabilization [34,35], it is important to study possible interaction(s) among other cytokines (e.g., IL-6, tumor necrosis factor-α, IL-4, and IL-10), transforming growth factor-β, and insulin to delineate its role not only in cancer cachexia but also in other muscular atrophies/dystrophies, sepsis, obesity, diabetes mellitus, and the metabolic syndrome.
ISSN:0899-9007
1873-1244
DOI:10.1016/j.nut.2012.02.005