Programming towards Childhood Obesity

Abstract

There is now considerable evidence that a constitutional susceptibility to fat gain is necessary for children to become obese under the pressure of an obesogenic environment; this is the programming towards obesity. The role of genetics in this programming is dominant. Besides the rare monogenic recessive forms of obesity secondary to mutations in genes involved in the hypothalamic appetite control pathways, obesity linked to mutations in melanocortin 3 and 4 receptors are more frequent due to their dominant mode of transmission. Predisposition to common obesity is polygenic and involves a network of genes; nevertheless, more research is required to elucidate their exact role. Fetal and perhaps early postnatal programming is also possible. Under- and overnutrition, diabetes, and maternal smoking during pregnancy were shown to promote later obesity and may affect the central body weight regulatory system during fetal development. The role of early postnatal factors such as formula-feeding rather than breastfeeding, excess in n–6 polyunsaturated fatty acids or protein intakes, and excessive weight gain early in life is more questionable and needs further investigation. Taking into consideration that childhood obesity is a programmed disease should modify its clinical management. Childhood obesity should no longer be considered as the result of inappropriate eating habits and/or excessive inactivity in order to relieve the obese children’s discrimination and their parents’ guilt. Since treatment of obese children requires a substantial motivation to continuously fight against the programmed excessive drive to eat, it seems wiser to wait for children to be old enough, thus more motivated, to initiate energy restriction. Moreover, with the great majority of children being not predisposed to obesity, prevention strategies should not be addressed to the whole pediatric population but targeted to those children at risk. Improvement of knowledge on programming towards obesity is essential to develop more promising therapeutic and preventive approaches.

Vascular transcriptional alterations produced by juvenile obesity in Ossabaw swine

“…This is a product of the combinatorial effect of overnutrition and lack of physical activity, a set of behaviors facilitated by our society (20,38,47,79). Importantly, obesity during childhood has subsequently been linked with a variety of adverse health outcomes in adulthood, particularly coronary artery disease (34,42,54).…”

Effects of Ovariectomy and 17<i>β</i>-Estradiol Replacement on Dopamine D2 Receptors in Female Rats: Consequences on Sucrose, Alcohol, Water Intakes and Body Weight

“…It resulted from a dysfunction of the appetite normal regulation loop where an unbalance occurred between overeating and low energy expenditure, leading to fat accumulation [1]. Many studies were carried out for the understanding of mechanisms underlying food intake and weight gain.…”

Early Influences of Nutrition on Postnatal Growth

“…These observations lead us to the conclusion that regulation of mTORC1 signaling by amino acids controls whole-body energy metabolism, bodyweight and body composition. Therefore, the current knowledge on the physiological mechanisms regulating metabolism, growth and related outcomes relevant for health indicate the large potential that improved nutritional practice during early life can have on long-term disease prevention and well-being, a concept widely known as early nutritional programming of life-long health [17][18][19][20][21][22][23]. Results of a recent randomized intervention trial in human infants demonstrate the powerful effects of modifying protein supply on metabolic and endocrine response as well as growth [24].…”