Abstract
In recent years, most research efforts have been focused on studying insulin-sensitizing adipokines. One of the most recently discovered adipokines is vaspin, a visceral adipose tissue-derived serine protease inhibitor. Vaspin levels have been found significantly increased in mice with obesity and insulin resistance. It has been assumed that vaspin serves as an insulin sensitizer with anti-inflammatory effects and might act as a compensatory mechanism in response to decreased insulin sensitivity. Most studies in humans have shown a positive correlation between vaspin gene expression and serum levels, and metabolic syndrome parameters. Vaspin gene expression is influenced by age and gender, and the administration of insulin sensitizers enhances it in mice, whereas the use of metformin decreases serum vaspin levels in humans, probably due to different regulatory mechanisms. Presumably vaspin plays local and endocrine role in the development of initial and advanced atherosclerosis in obese subjects and might be used as a predictor of coronary and cerebrovascular disease. It is believed that vaspin could be regarded as a new link between obesity and related metabolic disorders, including glucose intolerance. The entire understanding of vaspin intimate mechanism of action might enable the development of novel etiology-based treatment strategies, targeting metabolic and glucose tolerance disorders.
Highlights
Metabolic syndrome (MetS), defined as a set of cardiovascular disease and type 2 diabetes mellitus (T2DM) risk factors occurring together rather than separately, including abdominal obesity, increased fasting plasma glucose, hypertension, and dyslipidemia [1], underlies a number of socially significant diseases
Recombinant vaspin administration in DIO mice has significantly improved their glucose tolerance and insulin sensitivity. This beneficial effect results in normalizing plasma glucose levels and modifying the expression of genes involved in the pathogenesis of insulin resistance, such as resistin, leptin, TNFα, glucose transporter-4, and adiponectin. Based on these data it has been assumed that vaspin serves as an insulin sensitizer with anti-inflammatory effects and might act as a compensatory mechanism with target white adipose tissue (WAT), which is activated in response to the decreased insulin sensitivity [6, 7]
There is accumulating evidence that WAT-derived cytokines serve as mediators between obesity-related exogenous factors, such as diet and lifestyle, and the molecular mechanisms leading to MetS and inflammation and/or autoimmune conditions
Summary
Metabolic syndrome (MetS), defined as a set of cardiovascular disease and type 2 diabetes mellitus (T2DM) risk factors occurring together rather than separately, including abdominal obesity, increased fasting plasma glucose, hypertension, and dyslipidemia [1], underlies a number of socially significant diseases. Visceral adipose tissue (VAT) plays the role of fat depot, and appears to be an active endocrine organ that in the presence of obesity undergoes hyperplastic changes, involved in certain functions. It is responsible for a wide range of physiological processes, reproduction, apoptosis, inflammation, angiogenesis, blood pressure regulation, atherogenesis, coagulation, fibrinolysis, and immune and vascular homeostasis through direct or indirect impact on the regulation of proliferation. The biological mechanisms, underlying the detrimental impact of visceral fat accumulation, remain unclarified, it seems clear that adipokines might be of clinical importance in the treatment of MetS
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