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An estimated 2.1 billion adults and children worldwide are obese (1), imposing a substantial burden on people’s personal health and on society as a whole, as excess adiposity is associated with a number of cardiometabolic complications. These include insulin resistance, dyslipidemia, and hypertension, each of which is a risk factor for type 2 diabetes (T2D) and cardiovascular disease (CVD) (2,3). However, a sizeable proportion of obese individuals does not have these cardiometabolic complications. These individuals have favorable glucose, lipid, blood pressure, liver enzyme, hormone, and inflammation levels, despite their excess adiposity. Conversely, not all normal-weight individuals are healthy, as some demonstrate one or more cardiometabolic risk factors. Although there is no consensus on the criteria to define these obese and normal-weight subtypes, an estimated 15–45% of obese individuals are considered “metabolically healthy obese” (MHO) and 5–30% of the normal-weight population is considered “metabolically obese of normal weight” (MONW) (4–10).While interest in MHO and MONW populations is growing rapidly, it remains unclear which factors determine why some obese individuals are protected, and why some normal-weight individuals are at elevated risk. Age, sex, ethnicity/race, physical activity, smoking, and alcohol intake have been identified as important correlates of MHO and MONW (6–10). However, even after accounting for these factors, the MHO population continues to be protected (longer) from the development of cardiometabolic disease compared with other obese individuals, and the MONW population remains at greater risk than healthy people of normal weight (9–15). These observations suggest that innate physiological mechanisms underlie at least part of one’s predisposition to be MHO or MONW. Indeed, based on data from studies that were conducted mainly in rodent models, pathways implicated in adipogenesis, adipose tissue expandability, …

diabetes

Integrating Publicly Available Genome-Wide Association Data to Study the Genetic Basis of Metabolically Healthy Obese and Metabolically Obese but Normal-Weight Individuals