Department of Nutrition,Midwestern State University - UNICENTRO,03 Simeão Camargo Varela de Sá Street, Vila Carli, Guarapuava, Paraná,Brazil.
Division of Palliative Care Medicine,Department of Oncology,University of Alberta, 11560 University Avenue,Edmonton, Alberta,Canada.
Proc Nutr Soc. 2018 Nov;77(4):394-402. doi: 10.1017/S0029665118000186. Epub 2018 Apr 30.
Cancer-associated malnutrition is driven by reduced dietary intake and by underlying metabolic changes (such as inflammation, anabolic resistance, proteolysis, lipolysis and futile cycling) induced by the tumour and activated immune cells. Cytotoxic and targeted chemotherapies also elicit proteolysis and lipolysis at the tissue level. In this review, we summarise specific mediators and chemotherapy effects that provoke excess proteolysis in muscle and excess lipolysis in adipose tissue. A nutritionally relevant question is whether and to what degree these catabolic changes can be reversed by nutritional therapy. In skeletal muscle, tumour factors and chemotherapy drugs activate intracellular signals that result in the suppression of protein synthesis and activation of a transcriptional programme leading to autophagy and degradation of myofibrillar proteins. Cancer nutrition therapy is intended to ensure adequate provision of energy fuels and a complete repertoire of biosynthetic building blocks. There is some promising evidence that cancer- and chemotherapy-associated metabolic alterations may also be corrected by certain individual nutrients. The amino acids leucine and arginine provided in the diet at least partially reverse anabolic suppression in muscle, while n-3 PUFA inhibit the transcriptional activation of muscle catabolism. Optimal conditions for exploiting these anabolic and anti-catabolic effects are currently under study, with the overall aim of net improvements in muscle mass, functionality, performance status and treatment tolerance.
癌症相关的营养不良是由肿瘤和激活的免疫细胞引起的饮食摄入减少和潜在代谢变化（如炎症、合成代谢抵抗、蛋白水解、脂肪分解和无效循环）驱动的。细胞毒性和靶向化疗也会在组织水平引发蛋白水解和脂肪分解。在这篇综述中，我们总结了特定的介质和化疗作用，这些作用会导致肌肉中过度的蛋白水解和脂肪组织中过度的脂肪分解。一个与营养相关的问题是，这些分解代谢变化是否可以通过营养治疗来逆转，以及在多大程度上可以逆转。在骨骼肌中，肿瘤因子和化疗药物激活细胞内信号，导致蛋白质合成抑制和转录程序激活，从而导致自噬和肌原纤维蛋白降解。癌症营养治疗旨在确保提供足够的能量燃料和完整的生物合成构建块。有一些有希望的证据表明，癌症和化疗相关的代谢改变也可以通过某些特定的营养素来纠正。饮食中提供的氨基酸亮氨酸和精氨酸至少部分逆转了肌肉中的合成代谢抑制，而 n-3PUFA 抑制了肌肉分解代谢的转录激活。目前正在研究利用这些合成代谢和抗分解代谢作用的最佳条件，总体目标是改善肌肉质量、功能、身体状况和治疗耐受性。
