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Leptin in Anorexia and Cachexia Syndrome

机译:瘦素在厌食症和恶病质综合症中的作用

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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.
机译:瘦素是肥胖细胞(OB)基因与脂肪细胞成比例分泌的产物。它通过影响食源性和厌食性下丘脑途径之间的平衡而减少食物摄入并增加能量消耗。瘦素水平低是导致卡路里缺乏后食欲和体重补偿性增加以及能量消耗(EE)降低的原因。厌食症-恶病质综合征是许多慢性疾病的并发症,包括癌症,慢性阻塞性肺疾病,充血性心力衰竭,慢性肾脏疾病和衰老,其中体重和食物摄入量减少后没有食欲或体重的代偿性增加。 EE降低。矛盾的是瘦素与已知在这些情况下被激活的炎症信号之间的串扰。该手稿将回顾在与慢性病有关的厌食和恶病质中,瘦素途径发生改变的证据和潜在机制。

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