Adipokines, Inflammation, and Atherosclerosis

Obesity is the epidemic challenging our society from a medical as well as an economic perspective. The prevalence of obesity leading to decreased life expectancy due to, e.g., cardiovascular disease is dramatically escalating. In the UK, for instance, rat

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14

Thomas M. Stulnig and Maximilian Zeyda

14.1

Introduction: Obesity and Atherosclerosis Are Inflammatory Conditions Driven by Adipokines

Obesity is the epidemic challenging our society from a medical as well as an economic perspective. The prevalence of obesity leading to decreased life expectancy due to, e.g., cardiovascular disease is dramatically escalating. In the UK, for instance, rates of obese (body-mass index 30 kg/m2) have increased by 30% in women, 40% in men, and 50% in children within the last decade resulting in 23% of adults being obese in 2007 and a prognosis of 50% for 2050 [1]. The causes underlying the obesity epidemic are still not entirely understood, but its consequences are already apparent, e.g. by the dramatic increase in type 2 diabetes (T2DM), a disease complicated by increased risk of macrovascular and microvascular disease, nowadays even occurring in children [2]. Obesity is the outstanding risk factor for insulin resistance that results in the metabolic syndrome and its features and sequelae such as dyslipidemia, hypertension, T2DM and cardiovascular disease [3–7]. The latter relationship is most crucial bearing in mind that 80% of people with T2DM will die from the complications of cardiovascular disease resulting in an increased risk of death equivalent to 15 years of aging [8]. In recent years, more and more evidence has emerged that obesity is associated with a chronic low-grade inflammation as determined by increased plasma levels of C-reactive protein [9, 10], inflammatory cytokines such as tumor necrosis factor (TNF)-a [11], interleukin (IL)-6 [12], monocyte chemotactic protein (MCP)-1 [13], and IL-8 [14], and the multifunctional proteins osteopontin [15, 16] and leptin [17]. The primary source of elevated circulating cytokines in obesity-associated inflammation has been shown to be the adipose tissue [18, 19]. The adipose tissue,

T.M. Stulnig (*) • M. Zeyda Department of Medicine III, Clinical Division of Endocrinology and Metabolism, Medical University of Vienna, Vienna, Austria e-mail: [email protected] G. Wick and C. Grundtman (eds.), Inflammation and Atherosclerosis, DOI 10.1007/978-3-7091-0338-8_14, # Springer-Verlag/Wien 2012

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although previously regarded as a mere energy storage organ, is by now well recognized as an endocrine organ, which secretes a number of mediator molecules with diverse biological functions, collectively called adipokines [20]. Adipokines have important autocrine/paracrine roles in regulating adipocyte differentiation (adipogenesis), lipid and glucose metabolism, inflammatory responses [21, 22] as well as cardiovascular functions [23]. Hence, the role of adipokines goes far beyond metabolic homeostasis, particularly in obesity, when secretion of essentially all known adipokines including inflammatory cytokines is severely altered. Within the obese adipose tissue, macrophages drive inflammation by mechanisms not perfectly understood yet [24–27]. The attraction of macrophages is possibly trigge

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