LAUSR

Obesity, a major risk factor for type 2 diabetes, has become a global epidemic and represents an urgent research and medical topic. Rates of overweight and obesity continue to grow both in adults and children. Importantly, according to the concept of fetal programing, the development of obesity has an origin very early in life, starting in utero, as a result of metabolic or nutrient stress in pregnant mothers. Moreover, the fetal origin of adult diseases theory implicates the contribution of the early environment in the womb to the development of various diseases such as cardiovascular disease and diabetes in later life. Finally, the pandemic of COVID-19 may further aggravate the obesity problem due to lockdowns, remote working/schooling, a more sedentary style of living, reduced physical activity, and increased consumption of an unhealthy diet in excess of need. Thus, obesity is also a major societal challenge, which requires a multidisciplinary approach. This Research Topic entitled “Fetal Origin of Obesity and Diabetes” covered a variety of aspects of obesity (from basic science, through clinical studies to treatment and intervention approaches). Here we focus on the following topics: 1) fetal programming of obesity, 2) sexual dimorphic effects of obesity, and 3) interventions and treatment strategies in children. This Research Topic consists of five original articles, one review, and one mini-review. The first original paper by Qian Zhang et al. 1 focused on long-term effects of intrauterine energy intake on brown adipose tissue (BAT) metabolism in adulthood. To achieve this goal, high-fat diet (HFD) were given to mouse dams before and during pregnancy and lactation. The authors employed histological techniques using hematoxylin and eosin standing and DNA methylation arrays to assess the genome-wide methylation profile of BAT. They concluded that maternal HFD leads to long-lasting alterations of BAT in offspring. These changes include the activation of BATspecific genes important for fatty acid oxidation and thermogenesis via DNA methylation. In the second original paper by Annelene Govindsamy et al. 2 expression profiles of factors in the neonatal female, and male whole neonatal rat hearts were studied in response to varying dietary fat content. First, they performed immunohistochemistry for insulin receptor, glucose transporter 4 (Glut4), and forkhead box protein 1 (FoxO1) in whole hearts of neonates from dams fed with 10%, 20%, 30% or 40% high fat diet. They also examined expression levels of 84 genes, involved in the insulin signaling pathway in 10% or 40% neonates. Overall, this study shows that maternal diet may