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Role of NO/VASP Signaling Pathway against Obesity-Related Inflammation and Insulin Resistance
Article in English | WPRIM (Western Pacific) | ID: wpr-110922
Responsible library: WPRO
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.
Subject(s)

Full text: Available Database: WPRIM (Western Pacific) Main subject: Insulin Resistance / Endothelium, Vascular / Cardiovascular Diseases / Adipose Tissue / Diabetes Mellitus, Type 2 / Dyslipidemias / Pandemics / Glucose / Inflammation / Insulin Language: English Journal: Diabetes & Metabolism Journal Year: 2017 Document type: Article
Full text: Available Database: WPRIM (Western Pacific) Main subject: Insulin Resistance / Endothelium, Vascular / Cardiovascular Diseases / Adipose Tissue / Diabetes Mellitus, Type 2 / Dyslipidemias / Pandemics / Glucose / Inflammation / Insulin Language: English Journal: Diabetes & Metabolism Journal Year: 2017 Document type: Article
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