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

Diabetes & Metabolism Journal

Yu Mi Kang¹  Woo Je Lee¹  Francis Kim² 

[1] Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.;Department of Medicine, Diabetes and Obesity Center of Excellence, University of Washington, Seattle, WA, USA.;

关键词: Adipose tissue;    Chronic inflammation;    Endothelium, vascular;    Insulin resistance;    Liver;    Macrophages;    Nitric oxide;    Obesity;    Vasodilator-stimulated phosphoprotein;   

DOI  :  10.4093/dmj.2017.41.2.89

来源: DOAJ

【 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.

【 授权许可】

Unknown