Leptin in anorexia and cachexia syndrome.
Leptin in anorexia and cachexia syndrome.
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DOI：
10.1155/2012/287457
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发表时间：
2012
期刊：
影响因子：
--
通讯作者：
Garcia JM
中科院分区：
文献类型：
--
作者：
Engineer DR;Garcia JM
瘦素是脂肪细胞分泌的肥胖（OB）基因的产物，与脂肪量成正比。它通过影响食欲和厌食下丘脑途径之间的平衡来减少食物摄入并增加能量消耗。瘦素水平低是导致热量剥夺后食欲和体重代偿性增加以及能量消耗（EE）减少的原因。厌食-恶病质综合征是许多慢性疾病的并发症，包括癌症、慢性阻塞性肺病、充血性心力衰竭、慢性肾病和衰老，其中体重和食物摄入量的减少并没有伴随着食欲的代偿性增加或能量效率的降低。已知在这些情况下被激活的瘦素和炎症信号之间的串扰可能是造成这种悖论的原因。本手稿将回顾在与慢性疾病相关的厌食症和恶病质的情况下介导瘦素通路变化的证据和潜在机制。
Leptin is a product of the obese (OB) gene secreted by adipocytes in proportion to fat mass. It decreases food intake and increases energy expenditure by affecting the balance between orexigenic and anorexigenic hypothalamic pathways. Low leptin levels are responsible for the compensatory increase in appetite and body weight and decreased energy expenditure (EE) following caloric deprivation. The anorexia-cachexia syndrome is a complication of many chronic conditions including cancer, chronic obstructive pulmonary disease, congestive heart failure, chronic kidney disease, and aging, where the decrease in body weight and food intake is not followed by a compensatory increase in appetite or decreased EE. Crosstalk between leptin and inflammatory signaling known to be activated in these conditions may be responsible for this paradox. This manuscript will review the evidence and potential mechanisms mediating changes in the leptin pathway in the setting of anorexia and cachexia associated with chronic diseases.