1. Figure 1 Regulation of the ‘metabolically healthy obese’ phenotype
Figure 1 | Regulation of the 'metabolically healthy obese' phenotype. Body fat distribution and weight gain are regulated by complex genetic and epigenetic mechanisms that are probably governed by unique sets of developmental genes with tissue-specific expression, operating even in utero. This genetic regulation, together with cues for energy balance, dictates the adiposity status of an individual throughout life. Chronically overweight children with a sustained positive energy balance adapt their adipose tissue depots to store excess fat, whereas in the non-obese child such priming of adipose tissue does not occur. Upon exposure to the toxic environment of calorific excess in adulthood, these two backgrounds are likely to make a difference. Childhood priming (carrying favourable adiposity alleles or obesity risk gene variants in general) probably serves as a protection mechanism against complications of obesity, such as type 2 diabetes mellitus. In adult individuals without childhood priming, a premature crossing of the individual fat threshold for adipose tissue expandability occurs. MHO, metabolically healthy obesity; MUO, metabolically unhealthy obesity.
Vasan, S. K. & Karpe, F. (2016) Fat, yet fit
Nat. Rev. Endocrinol. doi: /nrendo