Pathophysiology and treatment of inflammatory anorexia in chronic disease.
Pathophysiology and treatment of inflammatory anorexia in chronic disease.
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DOI：
10.1007/s13539-010-0015-1
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发表时间：
2010-12
期刊：
影响因子：
--
通讯作者：
Marks DL
中科院分区：
文献类型：
--
作者：
Braun TP;Marks DL
食欲下降和非自愿体重减轻是慢性疾病中常见的现象，对生活质量和最终死亡率都有负面影响。慢性疾病中的体重减轻来自脂肪和瘦体重，被称为恶病质。食欲和体重减轻的改变发生在各种各样的疾病中，包括癌症、心力衰竭、肾衰竭、慢性阻塞性肺病和艾滋病毒。循环炎性细胞因子的增加被认为是恶病质和相关厌食症的共同致病机制。炎症介质的靶点之一是中枢神经系统，特别是位于腹侧间脑的下丘脑中的摄食中心。目前的研究已经开始阐明炎症到达下丘脑的机制，以及炎症性厌食症的神经基质。对这些神经机制的研究提出了新的治疗可能性，在临床前和临床试验中产生了有希望的结果。这篇综述将讨论下丘脑中介导厌食症的炎症信号，以及这些机制所提供的治疗干预的机会。
Decreased appetite and involuntary weight loss are common occurrences in chronic disease and have a negative impact on both quality of life and eventual mortality. Weight loss in chronic disease comes from both fat and lean mass, and is known as cachexia. Both alterations in appetite and body weight loss occur in a wide variety of diseases, including cancer, heart failure, renal failure, chronic obstructive pulmonary disease and HIV. An increase in circulating inflammatory cytokines has been implicated as a uniting pathogenic mechanism of cachexia and associated anorexia. One of the targets of inflammatory mediators is the central nervous system, and in particular feeding centers in the hypothalamus located in the ventral diencephalon. Current research has begun to elucidate the mechanisms by which inflammation reaches the hypothalamus, and the neural substrates underlying inflammatory anorexia. Research into these neural mechanisms has suggested new therapeutic possibilities, which have produced promising results in preclinical and clinical trials. This review will discuss inflammatory signaling in the hypothalamus that mediates anorexia, and the opportunities for therapeutic intervention that these mechanisms present.
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