RESUMO
OBJECTIVE: Muscle wasting contributes to the reduced quality of life and increased mortality in chronic obstructive pulmonary disease (COPD). Muscle atrophy in mice with cachexia was caused by Activin A binding to ActRIIB. The role of circulating Activin A leading to muscle atrophy in COPD remains elusive. METHODS: In the present study, we evaluated the relationship between serum levels of Activin A and skeletal muscle wasting in COPD patients. The expression levels of serum Activin A were measured in 78 stable COPD patients and in 60 healthy controls via ELISA, which was also used to determine the expression of circulating TNF-α levels. Total skeletal muscle mass (SMM) was calculated according to a validated formula by age and anthropometric measurements. The fat-free mass index (FFMI) was determined as the fat-free mass (FFM) corrected for body surface area. RESULTS: Compared to the healthy controls, COPD patients had upregulated Activin A expression. The elevated levels of Activin A were correlated with TNF-α expression, while total SMM and FFMI were significantly decreased in COPD patients. Furthermore, serum Activin A expression in COPD patients was negatively associated with both FFMI and BMI. CONCLUSION: The above results showed an association between increased circulating Activin A in COPD patients and the presence of muscle atrophy. Given our previous knowledge, we speculate that Activin A contributes to skeletal muscle wasting in COPD.
Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Idoso , Atrofia Muscular/etiologia , Doença Pulmonar Obstrutiva Crônica/complicações , Ativinas/sangue , Caquexia/metabolismo , Atrofia Muscular/metabolismo , Atrofia Muscular/sangue , Índice de Massa Corporal , Estudos de Casos e Controles , Fator de Necrose Tumoral alfa/metabolismo , Fator de Necrose Tumoral alfa/sangue , Músculo Esquelético/fisiopatologia , Doença Pulmonar Obstrutiva Crônica/sangue , Ativinas/metabolismo , Subunidades beta de InibinasRESUMO
Cancer cachexia causes disruption of lipid metabolism. Since it has been well established that the various adipose tissue depots demonstrate different responses to stimuli, we assessed the effect of cachexia on some biochemical and morphological parameters of adipocytes obtained from the mesenteric (MES), retroperitoneal (RPAT), and epididymal (EAT) adipose tissues of rats bearing Walker 256 carcinosarcoma, compared with controls. Relative weight and total fat content of tissues did not differ between tumor-bearing rats and controls, but fatty acid composition was modified by cachexia. Adipocyte dimensions were increased in MES and RPAT from tumor-bearing rats, but not in EAT, in relation to control. Ultrastructural alterations were observed in the adipocytes of tumor-bearing rat RPAT (membrane projections) and EAT (nuclear bodies)
Assuntos
Animais , Masculino , Ratos , Adipócitos/metabolismo , Tecido Adiposo/citologia , Caquexia/metabolismo , Carcinoma 256 de Walker/metabolismo , Adipócitos/ultraestrutura , Tecido Adiposo/metabolismo , Caquexia/patologia , Carcinoma 256 de Walker/patologia , Epididimo/citologia , Epididimo/metabolismo , Ácidos Graxos/análise , Lipídeos/análise , Mesentério/citologia , Mesentério/metabolismo , Peritônio/citologia , Peritônio/metabolismo , Proteínas/análise , Ratos Wistar , Espaço RetroperitonealRESUMO
The present review concerns metabolic alterations related to the establishment of cancer cachexia, a condition of extensive catabolism, responsible, in a great percentage of the cases, for the death of the patient. A brief review on the condition is presented and two major aspects of the host's altered metabolism are considered: the diminished plasma levels of insulin, triggering the catabolic mechanisms; and the reduced carnitine palmitoyltransferase II activity in hepatic mitochondria, rendering the liver unable of oxidizing fatty acids and of synthesizing ketone bodies. These modifications lead to the intensification of the wasting process and thus, from our point of view, might play an important role for the treatment of patients with neoplastic disease.
Assuntos
Humanos , Animais , Caquexia/metabolismo , Fígado/metabolismo , Neoplasias/complicações , Caquexia/etiologia , Carnitina O-Palmitoiltransferase , Insulina/sangue , Neoplasias/metabolismoRESUMO
La nutrición juega papel importante en la historia natural del cáncer. La dieta está involucrada en la carcinogénesis a través de mecanismos que son cada vez más claros. Se considera que por lo menos el 35 por ciento del total de casos de cáncer se asocian a la dieta y que cáncer y caquexia están entre las causas más comunes de muerte por enfermedad maligna. Esta revisión tiene el propósito de mostrar la relación del cáncer con la nutrición desde sus cuatro perspectivas: 1. La dieta como factor etiológico; 2. Las alteraciones nutricias causadas por la enfermedad; 3. Las alteraciones nutricias causadas por los tratamientos; y La alimentación del paciente con cáncer. Destacado además, la importancia que tiene la terapia nutricia en este especial grupo de pacientes.
Assuntos
Humanos , Lipídeos/metabolismo , Neoplasias/metabolismo , Ciências da Nutrição , Caquexia/dietoterapia , Caquexia/metabolismo , Comportamento Alimentar , Neoplasias/terapia , Avaliação NutricionalRESUMO
La nutrición convencional ha producido exitos limitados en la reducción de la morbilidad y de la mortalidad de los pacientes con cáncer. Un conocimiento mayor de los mecanismos de la caquexia en el cáncer es claramente necesario. Además, se debe desarrollar un enfoque innovativo del manejo metabólico y nutricional de los pacientes con cáncer para invertir los efectos catabólicos progresivos del estado tumoral. Mas, sin embargo, la ciencia básica y la investigación clínica son requeridos en el futuro para desarrollar un planteamiento selectivo y exitoso para el tratamiento de la caquexia por cáncer.