Obesity is clearly associated with chronic diseases such as type 2 diabetes, coronary heart disease, and dyslipidemia, yet the underlying mechanisms are not well defined. However, the evidence is strong that insulin resistance contributes greatly to the pathophysiology of these observed metabolic abnormalities and their associated morbidity (72). Insulin resistance is observed frequently in obese subjects and is considered an independent risk factor for the development of both type 2 diabetes and coronary artery disease (72-75). Although it is established that hyperinsulinemia, insulin resistance, and other obesity-related metabolic abnormalities are significantly associated with overall accumulation of fat in the body, there is considerable evidence that the specific fat distribution is important.
Excessive accumulation of fat in the upper body's abdominal area is referred to as ''truncal'' or ''central'' obesity. Central obesity appears to be a better predictor of morbidity than excess fat in the lower body, the so-called lower body segment obesity (72,74,75). Such types of body composition have been clinically separated based on a waist-to-hip circumference ratio (WHR) and individuals are referred to as having apple- or pear-shaped bodies, based on having an elevated or decreased WHR, respectively. The importance of body composition was first reported over 40 years ago by Vague, who noted that the incidence of metabolic complications among equally obese subjects varied depending on their physique (76). Morbidity was clearly shown to be higher in ''android-type'' obesity than in ''gynoid-type'' obesity and this heterogeneity was supported by results in several studies suggesting regional differences in adipose tissue metabolism (77-79). The heterogeneity of fat distribution has led investigators to accept the concept of morbid regional adiposity (i.e., that accumulation of fat in certain adipose tissue regions appears to be more deleterious than accumulation of fat in other adipose tissue regions). The hypothesis that has been put forward is that mesen-teric adipose tissues constitute the morbid areas of the body and accumulation of fat in these regions has major implications for metabolism and particularly for insulin sensitivity (72,74,75).
Specific abdominal fat depots do appear to have clinical relevance and efforts have been directed to assessing quantity of these fat depots by precise methods. Sonography has been used to measure intra-abdominal tissue (80,81), but has not been as widely used in clinical research settings as magnetic resonance imaging (MRI) and computer tomography (CT) scans. Both CT scans and MRI allow direct visualization of internal adipose tissue compartments and have been tested and validated in human subjects for assessment of intra-abdominal fat stores (82). The quantity of intra-abdominal fat, as assessed with MRI and CT scans, is significantly correlated to insulin resistance (83,84). In particular, it was observed in studies evaluating the insulin resistance of aging that insulin resistance related more to the visceral fat depot than to the subcutaneous fat depot (84). Additional studies have evaluated adipose tissue distribution in other areas, such as thigh skeletal muscle, and have shown significant correlation to insulin sensitivity (85). Thus, it is well established that obesity, in particular central obesity, appears to be the depot most associated with insulin resistance.
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