Role of NO/VASP Signaling Pathway against Obesity-Related Inflammation and Insulin Resistance

被引:25
作者
Kang, Yu Mi [1 ]
Kim, Francis [2 ]
Lee, Woo Je [1 ]
机构
[1] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Internal Med, 88 Olymp Ro 43 Gil, Seoul 05505, South Korea
[2] Univ Washington, Dept Med, Diabet & Obes Ctr Excellence, Seattle, WA USA
关键词
Adipose tissue; Chronic inflammation; Endothelium; vascular; Insulin resistance; Liver; Macrophages; Nitric oxide; Obesity; Vasodilator-stimulated phosphoprotein; VASODILATOR-STIMULATED PHOSPHOPROTEIN; DIETARY INORGANIC NITRATE; KUPFFER CELL ACTIVATION; NITRIC-OXIDE; ADIPOSE-TISSUE; VASCULAR INFLAMMATION; MACROPHAGE INFILTRATION; ENDOTHELIAL-CELLS; CANCER CELLS; CONTRIBUTES;
D O I
10.4093/dmj.2017.41.2.89
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Obesity has quickly become a worldwide pandemic, causing major adverse health outcomes such as dyslipidemia, type 2 diabetes mellitus, cardiovascular disease and cancers. Obesity-induced insulin resistance is the key for developing these metabolic disorders, and investigation to understand the molecular mechanisms involved has been vibrant for the past few decades. Of these, low-grade chronic inflammation is suggested as a critical concept in the development of obesity-induced insulin resistance, and the anti-inflammatory effect of nitric oxide (NO) signaling has been reported to be linked to improvement of insulin resistance in multiple organs involved in glucose metabolism. Recently, a body of evidence suggested that vasodilatory-stimulated phosphoprotein (VASP), a downstream mediator of NO signaling plays a crucial role in the anti-inflammatory effect and improvement of peripheral insulin resistance. These preclinical studies suggest that NO/VASP signaling could be an ideal therapeutic target in the treatment of obesity-related metabolic dysfunction. In this review, we introduce studies that investigated the protective role of NO/VASP signaling against obesity-related inflammation and insulin resistance in various tissues.
引用
收藏
页码:89 / 95
页数:7
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