Mechanisms of Glucocorticoid-Induced Insulin Resistance Focus on Adipose Tissue Function and Lipid Metabolism

被引：275
作者：
Geer, Eliza B. [1 ]
Islam, Julie [2 ]
Buettner, Christoph [1 ]
机构：
[1] Mt Sinai Med Ctr, Div Endocrinol, New York, NY 10029 USA
[2] Beth Israel Deaconess Med Ctr, Div Endocrinol & Metab, New York, NY 10003 USA
来源：
ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA | 2014年 / 43卷 / 01期
关键词：
Glucocorticoids; Cushing syndrome; Adipose tissue; Lipolysis; Lipids; Insulin resistance; 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-1; PITUITARY-ADRENAL AXIS; BODY-FAT DISTRIBUTION; TUMOR-NECROSIS-FACTOR; DE-NOVO LIPOGENESIS; MAGNETIC-RESONANCE-SPECTROSCOPY; NONALCOHOLIC HEPATIC STEATOSIS; SPLANCHNIC CORTISOL PRODUCTION; ENDOGENOUS CUSHINGS-SYNDROME; HORMONE-SENSITIVE LIPASE;
D O I：
10.1016/j.ecl.2013.10.005
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Glucocorticoids (GCs) are critical in the regulation of the stress response, inflammation and energy homeostasis. Excessive GC exposure results in whole-body insulin resistance, obesity, cardiovascular disease, and ultimately decreased survival, despite their potent anti-inflammatory effects. This apparent paradox may be explained by the complex actions of GCs on adipose tissue functionality. The wide prevalence of oral GC therapy makes their adverse systemic effects an important yet incompletely understood clinical problem. This article reviews the mechanisms by which supraphysiologic GC exposure promotes insulin resistance, focusing in particular on the effects on adipose tissue function and lipid metabolism.
引用
收藏
页码：75 / +
页数：29
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