Metabolic and Body Composition Factors in Subgroups of Obesity: What Do We Know?

Abstract

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.

Adipose tissue distribution and risk of metabolic disease: does thiazolidinedione-induced adipose tissue redistribution provide a clue to the answer?

“…In men, there is an increase in adipocyte number in the subcutaneous depot of the abdominal region, while this is not readily seen in women. Unlike obesity developed in childhood or adolescence, which is usually hyperplastic and is commonly seen in MHO subjects [1][2][3], most adult-onset obesity is related to the hypertrophic expansion of existing adipocytes, i.e. an increase in cell size [1,2].…”

“…Nevertheless, the level of risk differs among obese individuals; approximately 20% of people who meet the criteria for obesity are apparently insulin sensitive and metabolically normal, despite having large amounts of body fat. These individuals have been categorised as metabolically healthy but obese (MHO) subjects [3]. In contrast, there have also been reports that a considerable number of people, about 18% of the general population, are metabolically obese but have a normal body weight (MONW), i.e.…”

“…In contrast, there have also been reports that a considerable number of people, about 18% of the general population, are metabolically obese but have a normal body weight (MONW), i.e. they have a normal BMI or may be slightly overweight, but display several of the metabolic abnormalities associated with the metabolic syndrome [3]. Moreover, patients suffering from the lipodystrophy syndrome, which results in a partial to nearly total body fat loss, often have severely impaired insulin action and distorted metabolic profiles [4].…”

Is a nutritional therapeutic approach unsuitable for metabolically healthy but obese women?

“…These results are remarkable because they imply that treating all obese individuals using a nutritional approach might have a detrimental outcome in terms of insulin sensitivity in a considerable proportion (20-30%) [10]. These preliminary results highlight the need for studies to clarify whether an obese patient should be treated using a dietary approach.…”

Pharmacogenomic assessment of treatment options in gestational diabetes

“…ment of metabolic diseases, 29,30 one might speculate that these small but significant differences contribute to the pathological nature of intra-abdominal fat stores. Thus, the addition of insulin might attenuate the adverse effects of visceral adiposity in GDM patients by making visceral fat more like subcutaneous adipose.…”