The development of obesity begins early in life. From our large observational studies we know that the age between 3-6 years appears critical for development of obesity in children and once established, childhood obesity regularly persists into adulthood leading to premature morbidity and even mortality. In addition to the mere expansion of fat mass with developing childhood obesity, there are alterations in adipose tissue function such as adipocyte hypertrophy, inflammation and fibrosis in adipose tissue depots, and an imbalance in adipokine secretion. This adipose tissue dysfunction is related to, and likely to contribute to, the early manifestation of clinical obesity-related comorbidities already emerging in the children.
Epidemiological studies have identified parental overweight, social deprivation and perinatal factors followed by the classical life-style factors as major risk factors for childhood obesity. Nevertheless, the mechanisms remain incompletely understood and include interplay of genetic, epigenetic and environmental factors. We have studied the functional role for some of such factors at the level of the adipose tissue to better understand the mechanisms behind the mere risk associations for childhood obesity.
19 Sep 2019 - 21 Sep 2019