Mediators of cachexia in cancer patients.
Nutrition
; 66: 11-15, 2019 10.
Article
en En
| MEDLINE
| ID: mdl-31177056
ABSTRACT
Alterations in amino acid and protein metabolism-particularly in skeletal muscle-are a key feature of cancer that contributes to the cachexia syndrome. Thus, skeletal muscle protein turnover is characterized by an exacerbated rate of protein degradation, promoted by an activation of different proteolytic systems that include the ubiquitin-proteasome and the autophagic-lysosomal pathways. These changes are promoted by both hormonal alterations and inflammatory mediators released as a result of the systemic inflammatory response induced by the tumor. Other events, such as alterations in the rate of myogenesis/apoptosis and decreased regeneration potential also affect skeletal muscle in patients with cancer. Mitochondrial dysfunction also contributes to changes in skeletal muscle metabolism and further contributes to the exacerbation of the cancer-wasting syndrome. Different inflammatory mediators-either released by the tumor or by the patient's healthy cells-are responsible for the activation of these catabolic processes that take place in skeletal muscle and in other tissues/organs, such as liver or adipose tissues. Indeed, white adipose tissue is also subject to extensive wasting and "browning" of some of the white adipocytes into beige cells; therefore increasing the energetic inefficiency of the patient with cancer. Recently, an interest in the role of micromRNAs-either free or transported into exosomes-has been related to the events that take place in white adipose tissue during cancer cachexia.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Caquexia
/
Neoplasias
Límite:
Humans
Idioma:
En
Revista:
Nutrition
Asunto de la revista:
CIENCIAS DA NUTRICAO
Año:
2019
Tipo del documento:
Article