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

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 molec...

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Bibliographic Details
Published in:Diabetes & metabolism journal 2017, 41(2), 160, pp.89-95
Main Authors: Kang, Yu Mi, Kim, Francis, Lee, Woo Je
Format: Article
Language:English
Subjects:
Adipose tissue
Chronic inflammation
Endothelium, vascular
Insulin resistance
Liver
Macrophages
Nitric oxide
Obesity
Review
Vasodilator-stimulated phosphoprotein
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Summary: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.
ISSN:2233-6079
2233-6087
DOI:10.4093/dmj.2017.41.2.89