Role of NO/VASP Signaling Pathway against Obesity-Related Inflammation and Insulin Resistance.
- Author:
Yu Mi KANG
1
;
Francis KIM
;
Woo Je LEE
Author Information
- Publication Type:Review
- Keywords: Adipose tissue; Chronic inflammation; Endothelium, vascular; Insulin resistance; Liver; Macrophages; Nitric oxide; Obesity; Vasodilator-stimulated phosphoprotein
- MeSH: Adipose Tissue; Cardiovascular Diseases; Diabetes Mellitus, Type 2; Dyslipidemias; Endothelium, Vascular; Glucose; Inflammation*; Insulin Resistance*; Insulin*; Liver; Macrophages; Metabolism; Nitric Oxide; Obesity; Pandemics
- From:Diabetes & Metabolism Journal 2017;41(2):89-95
- CountryRepublic of Korea
- Language:English
- Abstract: 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.
