Phenotyping obesity: A focus on metabolically healthy obesity and metabolically unhealthy normal weight

Abstract

Over the past 4 decades, research has shown that having a normal body weight does not automatically imply preserved metabolic health and a considerable number of lean individuals harbour metabolic abnormalities typically associated with obesity. Conversely, excess adiposity does not always equate with an abnormal metabolic profile. In fact, evidence exists for the presence of a metabolically unhealthy normal weight (MUHNW) and a metabolically healthy obese (MHO) phenotype. It has become increasingly recognised that different fat depots exert different effects on the metabolic profile of each individual by virtue of their location, structure and function, giving rise to these different body composition phenotypes. Furthermore, other factors have been implicated in the aetiopathogenesis of the body composition phenotypes, including genetics, ethnicity, age and lifestyle/behavioural factors. Even though to date both MHO and MUHNW have been widely investigated and documented in the literature, studies report different outcomes on long‐term cardiometabolic morbidity and mortality. Future large‐scale, observational and population‐based studies are required for better profiling of these phenotypes as well as to further elucidate the pathophysiological role of the adipocyte in the onset of metabolic disorders to allow for better risk stratification and a personalised treatment paradigm.

The Fascinating Interplay between Growth Hormone, Insulin-Like Growth Factor-1, and Insulin

“…An entirely different situation is present in T2DM and obesity. In that situation, portal insulin levels are generally high due to insulin resistance [ 16 , 17 ]. However, despite the considerable body of evidence pointing to a possible relationship between the state of the adipose tissue depots and regulation of the somatotropic axis, to date the relationship between obesity and low GH status remains incompletely understood [ 18 ].…”

Impaired Remodeling of White Adipose Tissue in Obesity and Aging: From Defective Adipogenesis to Adipose Organ Dysfunction

“…Adipocyte size varies according to several factors, including sex and fat depot (lower in vWAT than in sWAT in women, but not in It is worth noting that the adipogenic capacity of sWAT is not only limited but also extremely variable among individuals, as shown by the existence of persons with obesity either with or without insulin resistance and components of the metabolic syndrome, including impaired glucose regulation, atherogenic dyslipidemia, and hypertension, despite the same body mass index (BMI). In addition to these two obese phenotypes, which are called metabolic unhealthy obese (MUO) and metabolic healthy obese (MHO), respectively [17,18], there are also lean phenotypes characterized by the presence or absence of metabolic derangement, i.e., the metabolic unhealthy normal weight (MUNW), also called metabolically obese normal weight [MONW], and the metabolic healthy normal weight (MHNW), respectively [19]. This indicates that it is not just a matter of absolute quantity of fat and shifts the focus on sWAT dysfunction and remodeling of fat depots, which is dependent on the individual capacity to expand and accommodate the surplus of energy [20].…”

Validation and assessment of psychometric properties of the Greek Eating Behaviors Assessment for Obesity (GR-EBA-O)

“…The requirement to personalize therapeutic interventions has rendered the phenotyping of obesity indispensable [12,13]. Research indicates that pathological eating behaviors can play a role in phenotyping obese individuals [14].…”