The presence of obesity-related metabolic disturbances varies widely among obese individuals. Accordingly, a unique subset of obese individuals has been described in the medical literature, which seems to be protected or more resistant to the development of metabolic abnormalities associated with obesity. These individuals, now known as 'metabolically healthy but obese' (MHO), despite having excessive body fatness, display a favorable metabolic profile characterized by high levels of insulin sensitivity, no hypertension as well as a favorable lipid, inflammation, hormonal, liver enzyme and immune profile. However, recent studies have indicated that this healthier metabolic profile may not translate into a lower risk for mortality. Mechanisms that could explain the favorable metabolic profile of MHO individuals are poorly understood. However, preliminary evidence suggests that differences in visceral fat accumulation, birth weight, adipose cell size and gene expression-encoding markers of adipose cell differentiation may favor the development of the MHO phenotype. Despite the uncertainty regarding the exact degree of protection related to the MHO status, identification of underlying factors and mechanisms associated with this phenotype will eventually be invaluable in helping us understand factors that predispose, delay or protect obese individuals from metabolic disturbances. Collectively, a greater understanding of the MHO individual has important implications for therapeutic decision making, the characterization of subjects in research protocols and medical education. Keywords: metabolically healthy but obese; insulin sensitivity; body composition; metabolic risk factors; cardiovascular diseases Introduction Obesity has been increasing at a rapid rate over the past decades and has now reached epidemic proportions. Recent data suggest that 65% of US adult are overweight (body mass index425 kg m À2) and 30% are obese (body mass index430 kg m À2).1 Obesity is associated with numerous metabolic complications such as Type 2 diabetes, dyslipidemia, hypertension, cardiovascular diseases and several forms of cancer. 2 The risk of developing obesity-related complications is proportional to the degree of obesity, and more specifically to android fat accumulation. 3 However, the presence of these obesity-related metabolic disturbances varies widely among obese individuals. 4,5 Accordingly, a unique subset of obese individuals has been described in the medical literature that seems to be protected or more resistant to the development of metabolic abnormalities associated with obesity. 6-12 These individuals, now known as 'metabolically healthy but obese' (MHO), despite having excessive body fatness, display favorable metabolic profiles characterized by high levels of insulin sensitivity, no hypertension, as well as favorable lipid, inflammation, hormonal, liver enzyme and immune profiles 7,9,[13][14][15] ( Figure 1). This phenomenon has also been observed in adolescents. 16 Despite a clinical awareness of the MHO individu...

Obesity is thought to be a heterogeneous disorder with several possible etiologies; therefore, by examining subtypes of obesity we attempt to understand obesity's heterogeneous nature. The purpose of this review was to investigate the roles of metabolic, body composition, and cardiovascular disease risk in subtypes of obesity. We briefly consider two subtypes of obesity that have been identified in the literature. One subset of individuals, termed the metabolically healthy, but obese (MHO), despite having large amounts of fat mass compared with at risk obese individuals shows a normal metabolic profile, but remarkably normal to high levels of insulin sensitivity. Preliminary evidence suggests that this could be due at least in part to lower visceral fat levels and earlier onset of obesity. A second subset, termed the metabolically obese, but normal weight (MONW), present with normal body mass index, but have significant risk factors for diabetes, metabolic syndrome, and cardiovascular disease, which could be due to higher fat mass and plasma triglycerides as well as higher visceral fat and liver content. We also briefly consider the potential role of adipose and gastrointestinal hormonal profiles in MHO and MONW individuals, which could lead to a better understanding of potential factors that may regulate their body composition. This information will eventually be invaluable in helping us understand factors that predispose to or protect obese individuals from metabolic and cardiovascular disease. Collectively, a greater understanding of the MHO and MONW individual has important implications for therapeutic decision making, the characterization of subjects in research protocols, and medical education.

Results of the present study indicate that postmenopausal women displaying the MHO phenotype also have a favorable inflammation profile as shown by lower CRP and alpha-1 antitrypsin levels compared with insulin-resistant women. This suggests that a lower inflammation state, as attested by low CRP levels, could play a role in the protective profile of the MHO individual, and this may be associated metabolically to a lower risk for cardiovascular disease.

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