ABSTRACT
The major site of fat accumulation is subcutaneous adipose tissue (SAT), which is considered the “good” fat. However, signicant adipose tissue accumulation has been found intraabdominally (i.e., visceral), as well as in the intrathoracic area (Figure 21.1).1 Visceral adipose tissue (VAT) could be up to 38% of total fat,2,3 whereas fat in the thorax is limited by the lack of space and is usually not more than 1%–2% of total fat (Table 21.1). Both VAT and intrathoracic adipose tissue are recognized as risk factors for cardiovascular and coronary artery disease stronger than obesity per se.4-6
It is now recognized that the adipose tissue is not only an energy storage tissue but also a metabolically active organ secreting a variety of biologically active mediators collectively called adipokines.7 VAT is associated with increased insulin resistance, dyslipidemia, glucose intolerance, and several pathologies such as diabetes and hypertension.8,9 Visceral adipocytes, when compared in vitro to subcutaneous adipocytes, have been shown to be more proinammatory and lipolytic10 and more resistant to insulin suppression of lipolysis.11 However, triglyceride deposition has been found as ectopic fat within cells of nonadipose tissue that normally contain only small amounts of fat. Magnetic resonance spectroscopy has highlighted the fact that ectopic fat accumulates mainly in liver, heart, and muscle and also in pancreas. This leads to the so-called cell lipotoxicity that is associated with hepatic and peripheral insulin resistance, β cell and cardiac dysfunction, explaining in part why ectopic fat accumulation increases cardiometabolic risk.
