Cancer cachexia (CC) is a complex syndrome of bodily wasting and progressive functional decline. Unlike starvation, cachexia cannot be reversed by increased energy intake alone. Nonetheless, targeted nutritional support is a necessary component in multimodal syndrome management. Due to the highly catabolic nature of cancer cachexia, amino acid supplementation has been proposed. Interestingly, leucine has been found to increase protein synthesis and decrease protein degradation via mTORC1 pathway activation. Multiple pre-clinical studies have explored the impact of leucine supplementation in cachectic tumor-bearing hosts. Here, we provide an overview of leucine’s proposed modes of action to preserve lean mass in cachexia and review the current pre-clinical literature related to leucine supplementation during CC. Current research indicates that a leucine-rich diet may attenuate CC symptomology; however, these works are difficult to compare due to methodological differences. There is need for further pre-clinical work exploring leucine’s potential ability to modulate protein turnover and immune response during CC, as well as the impact of additive leucine on tumor growth.

Cancer cachexia is a syndrome of progressive weight loss and muscle wasting occurring in many advanced cancer patients. Cachexia significantly impairs quality of life and increases mortality. Cardiac atrophy and dysfunction have been observed in patients with cachexia, which may contribute to cachexia pathophysiology. However, relative to skeletal muscle, little research has been carried out to understand the mechanisms of cardiomyopathy in cachexia. Here, we review what is known clinically about the cardiac changes occurring in cachexia, followed by further discussion of underlying physiological and molecular mechanisms contributing to cachexia-induced cardiomyopathy. Impaired cardiac contractility and relaxation may be explained by a complex interplay of significant heart muscle atrophy and metabolic remodeling, including mitochondrial dysfunction. Because cardiac muscle has fundamental differences compared to skeletal muscle, understanding cardiac-specific effects of cachexia may bring light to unique therapeutic targets and ultimately improve clinical management for patients with cancer cachexia.

Cancer cachexia is a multifactorial syndrome of body weight loss, muscle wasting, and progressive functional decline affecting many advanced cancer patients and leading to worsened clinical outcomes. Despite inherent limitations of many preclinical cachexia models, including large tumor burden, rapid tumor growth, and young age of animals, these animal models are widely used and imperative for the study of cachexia mechanisms and experimental therapeutics. However, there are currently no guidelines for reporting and representation of data in preclinical cachexia literature. We examined the current state of data reporting in publications using the colon-26 adenocarcinoma (C26) model of cachexia and compared statistical differences in reporting mechanisms using animals from our laboratory. We show that data reporting and representation in C26 preclinical cachexia literature is diverse, making comparison of study outcomes difficult. Further, different expression of body and tissue weights in our animals led to differential statistical significance, which could significantly alter data interpretation. This study highlights a need for consistent data reporting in preclinical cancer cachexia literature to effectively compare outcomes between studies and increase translatability to the human condition.