For many years, adipose tissue was considered a passive storage organ, but it is now clear that adipose tissue plays an active role in controlling energy balance. The metabolic alterations of adipose tissue that occur in obesity are numerous. These include an increased release of secretory molecules such as fatty acids, hormones, and proinflam-matory cytokines. Relative decreases in insulin receptor number and function lead to reduced insulin sensitivity, a condition that may contribute to altered fuel partitioning. It has been hypothesized that the insulin resistance associated with obesity may in fact be a protective/adaptive mechanism against further weight gain (17).
Adipose tissue produces metabolically active proinflammatory molecules called adipocytokines such as tumour necrosis factor (TNF)-a, interleukins (IL), leptin, adiponectin (18-20), and some newly identified molecules such as visfatin (21) and omentin (22). The cytokines within adipose tissue originate predominantly from in situ macrophages (23-25) but also from adipocytes and preadipocytes (26). The altered production of these molecules has characterized obesity as a state of chronic, low-grade inflammation (27), which may contribute to the development of insulin resistance and endothelial dysfunction (28-30). It is postulated that paracrine and endocrine communication between macrophages and adipocytes, mediated by cytokines and fatty acids, creates a positive feedback loop to aggravate inflammatory changes in adipose tissue (31). Although the adipocytokines are reviewed in detail in previous chapters in this book, it is important to briefly highlight these compounds here, as they appear to play a role in the pathophysiology of CVD (32).
The regulation of adipocytokines in adipose tissue is complex and many of these molecules work together in autocrine regulation. For example, the increase of transforming growth factor (TGF)-^1 production in adipose tissue can induce plasminogen activator inhibitor (PAI)-1 and TGF-^1 can also inhibit leptin production (33). An increase in TNF-a can trigger the previously mentioned cascade of events and can also inhibit adiponectin expression (34), which together reduce insulin sensitivity and unfavourably modify vascular function and increase lipolysis (35). Persistent inflammation also seems to play a role in congestive heart failure (CHF) by reducing cardiac contractility, inducing cardiac hypertrophy, and promoting apoptosis, a process that contributes to undesirable myocardial remodeling (36).
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