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【JCEM】皮质醇在代谢综合征中病理过程中的作用
http://jcem.endojournals.org/cgi/content/abstract/94/8/2692
Context: The metabolic syndrome (MetS) is a cluster of metabolic abnormalities that increase the risk for type 2 diabetes mellitus and vascular disease. The common characteristics of MetS and hypercortisolemic conditions such as Cushing’s syndrome (CS) suggest that the pathogenesis of MetS and central obesity might involve prolonged and excessive exposure to glucocorticoids. The present review summarizes the evidence on the potential role of cortisol in the pathogenesis of MetS and discusses new therapeutic approaches for these patients.
Evidence Acquisition: Using PubMed, we searched for publications during the last 20 yr regarding the possible pathogenetic role of cortisol in the development of MetS.
Evidence Synthesis: Emerging data suggest that patients with MetS show hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, which leads to a state of "functional hypercortisolism." The cause for this activation of the HPA axis remains uncertain but may be partly associated with chronic stress and/or low birth weight, which are both associated with increased circulating cortisol levels and greater responsiveness of the HPA axis. Increased exposure to cortisol contributes to increased fat accumulation in visceral depots. However, cortisol metabolism is not only centrally regulated. The action of 11β-hydroxysteroid dehydrogenase-1 at the tissue level also modulates cortisol metabolism. Increased 11β-hydroxysteroid dehydrogenase-1 activity in adipose tissue and liver might contribute to the development of several features of the MetS.
Conclusions: MetS shares many characteristics of CS, and cortisol might play a role in the development of MetS at both a central and a peripheral level. 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。 The Pathogenetic Role of Cortisol in the Metabolic Syndrome: A Hypothesis
皮质醇在代谢综合征发病中可能的作用
http://jcem.endojournals.org/cgi/content/abstract/94/8/2692
Context: The metabolic syndrome (MetS) is a cluster of metabolic abnormalities that increase the risk for type 2 diabetes mellitus and vascular disease. The common characteristics of MetS and hypercortisolemic conditions such as Cushing’s syndrome (CS) suggest that the pathogenesis of MetS and central obesity might involve prolonged and excessive exposure to glucocorticoids. The present review summarizes the evidence on the potential role of cortisol in the pathogenesis of MetS and discusses new therapeutic approaches for these patients.
背景：代谢综合征指的是一系列会增加2型糖尿病及血管疾病危险性的代谢异常。代谢综合征与高皮质醇状态，如cushing病具有某些类似特征，提示代谢综合征与中心型肥胖的发生可能与长期异常增加的皮质醇水平有关。本文综述了皮质醇参与代谢综合征发生的证据，并探讨了对该类患者治疗的新方法。
Evidence Acquisition: Using PubMed, we searched for publications during the last 20 yr regarding the possible pathogenetic role of cortisol in the development of MetS.
证据的获取：通过PUBMED检索，我们查阅了近20年来发表的有关皮质醇可能参与代谢综合征发病的文章。
Evidence Synthesis: Emerging data suggest that patients with MetS show hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, which leads to a state of "functional hypercortisolism." The cause for this activation of the HPA axis remains uncertain but may be partly associated with chronic stress and/or low birth weight, which are both associated with increased circulating cortisol levels and greater responsiveness of the HPA axis. Increased exposure to cortisol contributes to increased fat accumulation in visceral depots. However, cortisol metabolism is not only centrally regulated. The action of 11β-hydroxysteroid dehydrogenase-1 at the tissue level also modulates cortisol metabolism. Increased 11β-hydroxysteroid dehydrogenase-1 activity in adipose tissue and liver might contribute to the development of several features of the MetS.
证据的综合：数据显示代谢综合征患者的“下丘脑-垂体-肾上腺”轴（HPA）活性增加，导致出现所谓“功能性高皮质醇”。HPA轴活化的原因并不清楚，在一定程度上可能与慢性应激及低出生体重有关，因为后两者与血液中皮质醇水平升高及HPA轴高反应性俱有关系。皮质醇水平升高促进了内脏脂肪组织的脂质沉积。当然，皮质醇的调节并非仅受中枢调节。组织水平的11-beta羟类固醇脱氢酶 也会调节皮质醇的代谢。脂肪及肝脏组织11-beta羟类固醇脱氢酶活性增强也可能参与了代谢综合征某些特征的发生。
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作者:admin@医学,生命科学 2010-12-07 05:11
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