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恶病质与神经肽Y

Cachexia and neuropeptide Y.

作者信息

Morley John E, Farr Susan A

机构信息

Division of Geriatric Medicine, Saint Louis University School of Medicine, St. Louis, Missouri, USA.

出版信息

Nutrition. 2008 Sep;24(9):815-9. doi: 10.1016/j.nut.2008.06.020.

DOI:10.1016/j.nut.2008.06.020
PMID:18725077
Abstract

Cachexia or wasting disease occurs commonly in diseases that have an overproduction of proinflammatory cytokines associated with them. The hallmarks of cachexia are loss of lean and adipose tissue, anorexia, anemia, memory disturbance, and sickness behavior. This review suggests that increased inducible nitric oxide synthase production in the hypothalamus leads to severe anorexia and that this is the pathway through which proinflammatory cytokines produce anorexia. Orexigenic peptides, such as neuropeptide, ghrelin, and orexin A, and anorectic peptides, such as leptin, produce their effects through neuronal nitric oxide synthase. Activation of neuronal nitric oxide synthase results in increased adenosine monophosphate kinase and a decrease in malonyl coenzyme A, leading to increased food intake.

摘要

恶病质或消耗性疾病常见于伴有促炎细胞因子过度产生的疾病中。恶病质的特征包括瘦组织和脂肪组织丢失、厌食、贫血、记忆障碍和疾病行为。本综述表明,下丘脑诱导型一氧化氮合酶产生增加会导致严重厌食,这是促炎细胞因子产生厌食的途径。食欲肽,如神经肽、胃饥饿素和食欲素A,以及厌食肽,如瘦素,通过神经元型一氧化氮合酶发挥作用。神经元型一氧化氮合酶的激活导致腺苷单磷酸激酶增加和丙二酰辅酶A减少,从而导致食物摄入量增加。

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