Paredes Sílvia, Ribeiro Laura
Faculty of Medicine, University of Porto.
Department of Biochemistry and Center for Medical Education, Faculty of Medicine, University of Porto.
Rev Assoc Med Bras (1992). 2014 Jan-Feb;60(1):84-92. doi: 10.1590/1806-9282.60.01.017.
This article reviews the state of the art regarding the association between glucocorticoid actions and both obesity and insulin resistance, two main features of the metabolic syndrome.
A methodological assessment of the literature on PubMed and SciELO databases was conducted by using the following terms: stress, metabolic syndrome, glucocorticoids, obesity, insulin resistance, hypothalamic-pituitary-adrenal-axis and 11β-hydroxysteroid dehydrogenase.
Chronic stress, mainly through hypothalamic-pituitary-adrenal axis dysregulation, promotes the accumulation of visceral fat. Reciprocally, obesity promotes a systemic low-grade inflammation state, mediated by increased adipokine secretion, which can chronically stimulate and disturb stress system. This vicious cycle, probably initiated by visceral adipose tissue dysfunction, might be the trigger for the development of metabolic syndrome.
Given the strong evidences linking glucocorticoid release, obesity and type 2 diabetes, better understanding of the mechanisms underlying this connection might be useful for prevention and treatment of the metabolic syndrome.
本文综述了糖皮质激素作用与肥胖和胰岛素抵抗（代谢综合征的两个主要特征）之间关联的最新研究状况。
通过使用以下术语对PubMed和SciELO数据库中的文献进行方法学评估：应激、代谢综合征、糖皮质激素、肥胖、胰岛素抵抗、下丘脑-垂体-肾上腺轴和11β-羟基类固醇脱氢酶。
慢性应激主要通过下丘脑-垂体-肾上腺轴失调促进内脏脂肪堆积。反之，肥胖会促进全身性低度炎症状态，这是由脂肪因子分泌增加介导的，而脂肪因子分泌增加会长期刺激并扰乱应激系统。这个恶性循环可能由内脏脂肪组织功能障碍引发，可能是代谢综合征发展的触发因素。
鉴于有充分证据表明糖皮质激素释放、肥胖与2型糖尿病之间存在联系，更好地理解这种联系背后的机制可能有助于代谢综合征的预防和治疗。
