Influence of cortisol status on leptin secretion

被引:68
作者
Leal-Cerro A. [1 ,2 ,3 ]
Soto A. [1 ,2 ,3 ]
Martínez M.A. [1 ,2 ,3 ]
Dieguez C. [1 ,2 ,3 ]
Casanueva F.F. [1 ,2 ,3 ]
机构
[1] Department of Endocrinology, H.U. Virgen del Rocío, Sevilla
[2] Department of Medicine, Endocrine Area Complejo Hospitalario Universitario de Santiago, Santiago de Compostela
[3] Department of Physiology, University of Santiago, Santiago de Compostela
关键词
Cushing's syndrome; Glucocorticoid; Leptin; Obesity;
D O I
10.1023/A:1012903330944
中图分类号
学科分类号
摘要
The discovery of the adipocyte-produced hormone leptin has changed the field of obesity research and our understanding of energy homeostasis. It is now accepted that leptin is the afferent loop informing the hypothalamus about the states of fat stores, with hypothalamic efferents regulating appetite and energy expenditure. I addition, leptin has a role as a metabolic adaptator in overweight and fasting states. New and previously unsuspected neuroendocrine roles have emerged for leptin. Leptin participates in the expression of CRH in the hypothalamus, interacts at the adrenal level with ACTH, and is regulated by glucocorticoids. Since leptin and cortisol show an inverse circadian rhythm, it has suggested that a regulatory feedback is present. However glucocorticoids appears to play a modulatory, but not essential roles in generating leptin diurnal rhythm. Glucocortiocids act directly on the adipose tissue and increase leptin synthesis and secretion in humans. Leptin levels are markedly increased in Cushing's syndrome patients and in other pseudo-Cushing's syndrome states. Glucocorticoids appears to act as a key modulator of body weight and food intake, promoting leptin secretion by adipocytes, limiting central leptin induced effects and favoring those of the NPY. Furthermore the modulatory role of glucocorticoids could be altered in obesity, but the precise mode of action remains to be established. The relevance of this finding merits further studies.
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页码:111 / 116
页数:5
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