Cancer-associated cachexia is defined by systemic inflammation, bodyweight loss, adipose tissue remodeling, and muscle wasting. Interestingly, until nowadays, the etiology for this syndrome still unclear. It is well known that multiple factors can contribute to adipose tissue remodeling, and longitudinal studies show that adipose tissue is affected early in the course of this syndrome. During cancer cachexia, adipose tissue remodeling is associated with adipocyte atrophy, impairment of fatty acid turnover, inflammation, reorganization of the extracellular matrix, and increased thermogenic gene programming of adipose tissue. Another attractive pathway is the adipose tissue lipolysis, which is the catabolic process that is leading to the breakdown of triglycerides stored in adipocytes and the release of fatty acids and glycerol. This pathway is highly involved in the adipose tissue wasting during cancer cachexia. Whole-body deletion of the genes that encode the lipolytic enzymes attenuates the effects of the syndrome on the reduction of body fat and muscle mass. These sets of changes, in addition to metabolites derived from this process, may be the initial trigger of the sequence of events that result in the remodeling and consequent dysfunction of adipose tissue during cancer cachexia. Therefore, this review aimed to investigate the main morpho-functional events that are resulting in adipose tissue remodeling in the context of cancer-associated cachexia.

This paper reports on a quasi-experimental study that aimed to identify changes in muscle function (i.e., mobility, maximal walking speed, lower limb muscle strength, balance, and transfer capacity), cognition (i.e., executive function) and hemodynamic parameters of community-dwelling Brazilian older adults during a six-month multicomponent exercise program (MCEP). A total of 436 community-dwelling older adults performed functional, cognitive and hemodynamic assessments before and after a six-month MCEP. The program of exercise was performed twice a week over 26 weeks at moderate intensity. Results indicate that balance, mobility (i.e., usual and maximal walking speeds) and transfer capacity (p < 0.05) were significantly improved after the MCEP. Moreover, all hemodynamic parameters (i.e., systolic, diastolic and mean arterial pressures), except for heart rate (p > 0.05), were significantly reduced after the intervention. The current findings indicate that a six-month MCEP may provide physical and hemodynamic benefits in community-dwelling older adults. Nevertheless, our findings need to be confirmed in larger samples and better designed studies.

O exercício físico crônico ou o treinamento físico (TF) tem sido largamente utilizado nos últimos anos com finalidade terapêutica e preventiva em uma série de condições fisiopatológicas, incluindo doenças cardiovasculares. Além dos benefícios cardiovasculares, o TF modula a expressão elevada de citocinas pró-inflamatórias, atuando sobre o eixo neuroimunoendócrino. Atualmente, o quadro de insuficiência cardíaca crônica (ICC) tem sido reconsiderado como uma interação entre mecanismos hemodinâmicos, neurormonais, endócrinos e imunológicos. Esta resposta inflamatória anormal, incluindo a elevada expressão de citocinas pró-inflamatórias, tem sido proposta como responsável pela progressão e deterioração clínica na ICC. Neste quadro, a principal citocina envolvida no quadro fisiopatológico da ICC é o fator de necrose tumoral-alfa (TNF-alfa). Assim, o TF pode atuar no quadro de ICC de duas maneiras, melhorando o desempenho durante o exercício físico, bem como atenuando do quadro deletério de elevada concentração de citocinas pró-inflamatórias no sistema cardiovascular, podendo representar importante opção imunomodulatória e, desta forma, permitir melhora significativa no quadro clínico do paciente.

Adipose tissue not only possesses an important role in the storage of excess nutrients but also acts as a critical immune and endocrine organ. Researchers and clinicians now consider adipose tissue to be an active endocrine organ that secretes various humoral factors called "adipokines," which imparts important systemic metabolic effects, from food intake to glucose tolerance. Along with its production of specialized adipokines, adipose tissue also secretes proinflammatory cytokines that likely contributes to the low-level systemic inflammation that has become a hallmark of various metabolic syndrome-associated chronic pathologies, such as obesity and cancer cachexia. These systemic effects may be mediated by communication networks arising from the multitude of resident adipose cells, including adipocytes, endothelial cells, neuronal cells, stem cells and other precursors, and a wide variety of immune cell populations that recent studies have demonstrated play a crucial role in the development of adipose inflammation and systemic metabolic abnormalities. In this chapter, we detail various molecular pathways linking excess adipose lipid storage to chronic inflammation and review the current knowledge as to what triggers obesity-and cachexia-associated inflammation in adipose tissue. Finally, we describe how the cross talk between adipose tissue inflammation and the non-adipocyte resident cells present in tissue is involved in this metabolic disruption.