Department of Nutritional Sciences, Texas Tech University, Lubbock, TX, United States; Obesity Research Cluster, Texas Tech University, Lubbock, TX, United States.
Department of Nutritional Sciences, Texas Tech University, Lubbock, TX, United States.
Biochim Biophys Acta Mol Basis Dis. 2017 May;1863(5):1106-1114. doi: 10.1016/j.bbadis.2016.07.019. Epub 2016 Aug 4.
Obesity is a complex disease characterized by excessive expansion of adipose tissue and is an important risk factor for chronic diseases such as cardiovascular disorders, hypertension and type 2 diabetes. Moreover, obesity is a major contributor to inflammation and oxidative stress, all of which are key underlying causes for diabetes and insulin resistance. Specifically, adipose tissue secretes bioactives molecules such as inflammatory hormone angiotensin II, generated in the Renin Angiotensin System (RAS) from its precursor angiotensinogen. Accumulated evidence suggests that RAS may serve as a strong link between obesity and insulin resistance. Dysregulation of RAS also occurs in several other tissues including those involved in regulation of glucose and whole body homeostasis as well as insulin sensitivity such as muscle, liver and pancreas and heart. Here we review the scientific evidence for these interactions and potential roles for oxidative stress, inflammation and mitochondrial dysfunction in these target tissues which may mediate effects of RAS in metabolic diseases. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondrial Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases - edited by P. Hemachandra Reddy.
肥胖症是一种以脂肪组织过度扩张为特征的复杂疾病,是心血管疾病、高血压和 2 型糖尿病等慢性病的重要危险因素。此外,肥胖症是炎症和氧化应激的主要诱因,而炎症和氧化应激都是糖尿病和胰岛素抵抗的关键潜在原因。具体来说,脂肪组织会分泌生物活性分子,如血管紧张素 II 等炎症激素,这些激素是肾素血管紧张素系统(RAS)从其前体血管紧张素原生成的。越来越多的证据表明,RAS 可能是肥胖症和胰岛素抵抗之间的重要联系。RAS 的失调也发生在其他几种组织中,包括参与调节葡萄糖和全身稳态以及肌肉、肝脏和胰腺和心脏等胰岛素敏感性的组织。本文综述了这些相互作用的科学证据,以及氧化应激、炎症和线粒体功能障碍在这些靶组织中的潜在作用,这些作用可能介导 RAS 在代谢性疾病中的作用。本文是题为“糖尿病/肥胖症和危重病谱疾病中的氧化应激和线粒体功能-由 P. Hemachandra Reddy 编辑”的特刊的一部分。