Lundholm K, Edström S, Ekman L, Karlberg I, Scherstén T
Cancer Treat Rep. 1981;65 Suppl 5:79-83.
Cancer patients have increased insulin resistance in skeletal muscles and probably also in the liver. The insulin production in response to a glucose challenge is decreased. This is associated with decreased glucose uptake in peripheral tissues and increased gluconeogenesis from amino acids, lactate, and glycerol. The correlation between the insulin response to a glucose challenge and the activities of glycolytic and oxidative rate-limiting enzymes in muscle tissue suggests a common denominator for these metabolic alterations. The most prominent feature in alteration of lipid metabolism is a reduction of body fat, probably dependent on increased lipolysis. The released fatty acids are oxidized outside the tumor mass. Species characteristics may be important for the degree of hyperlipidemia. Wasting of the skeletal muscle mass is caused by decreased protein synthesis and probably increased degradation. Anorexia can induce but not entirely explain this altered protein metabolism. Decreased physical activity may be another important factor for the depressed protein synthesis. Total parenteral nutrition (TPN) improves the muscle protein synthesis. The mechanism behind increased fractional degradation of muscle proteins in vitro is not clear, but it may be coupled to increased cathepsin D activity.
癌症患者骨骼肌以及可能肝脏中的胰岛素抵抗增强。葡萄糖刺激后胰岛素分泌减少。这与外周组织葡萄糖摄取减少以及氨基酸、乳酸和甘油的糖异生增加有关。肌肉组织中对葡萄糖刺激的胰岛素反应与糖酵解和氧化限速酶活性之间的相关性表明这些代谢改变存在一个共同特征。脂质代谢改变的最显著特征是体脂减少，可能依赖于脂解增加。释放的脂肪酸在肿瘤块外被氧化。物种特性可能对高脂血症程度很重要。骨骼肌质量的消耗是由蛋白质合成减少以及可能的降解增加所致。厌食可诱发但不能完全解释这种蛋白质代谢改变。体力活动减少可能是蛋白质合成受抑制的另一个重要因素。全胃肠外营养（TPN）可改善肌肉蛋白质合成。体外肌肉蛋白质降解分数增加背后的机制尚不清楚，但可能与组织蛋白酶D活性增加有关。
