Exploiting the therapeutic potential of leptin signaling in cachexia.
Exploiting the therapeutic potential of leptin signaling in cachexia.
复制标题
开发瘦素信号传导在恶病质中的治疗潜力。
DOI：
10.1097/spc.0000000000000092
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发表时间：
2014
影响因子：
2.1
通讯作者：
Gertler,Arieh
中科院分区：
文献类型：
--
作者：
Mak,RobertH;Cheung,WaiW;Gertler,Arieh
Cachexia is prevalent among patients with chronic diseases such as cancer, chronic kidney disease (CKD), congestive heart failure, HIV infection, and chronic obstructive pulmonary disease (COPD)[1]. It is to be distinguished from malnutrition, which is defined as the consequence of insufficient food intake or an improper diet. Malnutrition is characterized by hunger, which is an adaptive response, whereas anorexia is prevalent in patients with wasting or cachexia [1, 2, 3]. Energy expenditure decreases as a protective mechanism in malnutrition, whereas it remains inappropriately high in cachexia or wasting [4]. In malnutrition, fat mass is preferentially lost and lean body mass and muscle mass is preserved. In cachexia or wasting, muscle is wasted and fat is relatively underutilized [5–7]. Restoring adequate food intake or altering the composition of the diet reverses malnutrition. Nutrition supplementation does not totally reverse cachexia or wasting [8, 9]. Longevity has consistently been observed in patients with CKD who have more muscle and/or fat, who report better appetite, and who eat more [1]. Although inadequate nutritional intake may contribute to the cachexia syndrome, recent evidence indicates that other factors, including systemic inflammation, perturbations of appetite-controlling hormones from reduced renal clearance, aberrant neuropeptide signaling, insulin and insulin-like growth factor resistance, and metabolic acidosis, may be important in the pathogenesis of the cachexia syndrome [1, 5, 7, 8, 10].
