The idea that there is heterogeneity among obese individuals in their risk for
disease is not new, and may have begun with the acknowledgement that the distinct
cardiovascular disease risk between males and females was influenced by their body
pattern of adipose tissue accumulation (i.e. predominantly in the upper body versus in
the lower body, respectively). Later came the debate on the pathophysiological
meaning of adipose tissue accumulation in visceral as opposed to subcutaneous depots
and even of distinct patterns of adipose tissue growth (hyperplasia versus hypertrophy).
More recently, epidemiological evidence has shown that individuals with similar
degrees of obesity may be at different ranges of metabolic abnormality and
cardiometabolic risk spectrum. In addition, many subjects not fulfilling the criteria for
obesity diagnosis share the same metabolic disturbances of some obese individuals.
Although, it has been discussed that healthy obese people will sooner or later become
unhealthy, the question on why some subjects attain a status of metabolic chaos earlier
than others (for the same obesity levels or adipose tissue amount) is still matter of
debate. In this chapter, we propose to discuss the contribution of obesity-related
inflammation – metabolic inflammation – as cause or consequence of different obesity
phenotypes, overviewing the main possible adipose tissue inflammation triggers.
Keywords: Adipocyte hypertrophy, Adipose tissue, Central obesity, Gut
microbiota, Inflammasome, Metabolic inflammation, Metabolically healthy obese
phenotype, Metabolically unhealthy normal-weight phenotype, Metabolically
unhealthy obese phenotype, Obesity phenotypes, Peripheral obesity, Persistent
organic pollutants, Sex hormones, Subcutaneous adipose tissue, Visceral adipose
tissue.
