Abstract

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.