Pediatric obesity: etiology and treatment

Abstract

This article reviews factors that contribute to excessive weight gain in children and outlines current knowledge regarding approaches for treating pediatric obesity. Most of the known genetic causes of obesity primarily increase energy intake. Genes regulating the leptin signaling pathway are particularly important for human energy homeostasis. Obesity is a chronic disorder that requires long-term strategies for management. The foundation for all treatments for pediatric obesity remains restriction of energy intake with lifestyle modification. There are few long-term studies of pharmacotherapeutic interventions for pediatric obesity. Bariatric surgical approaches are the most efficacious treatment but, because of their potential risks, are reserved for those with the most significant complications of obesity.

Figure 1

A Social-Ecological Model of Influences on Pediatric Obesity and its Treatment. Levels of environmental influence begin with the family environment and extend to larger spheres of influence, including peers as well as neighborhoods, schools, community, and national factors. Some of the influences within each of these spheres are also given. For examples, neighborhood environment may influence children’s activity if there are no sidewalks or if safe areas for play are not available. Figure courtesy of Denise E Wilfley, PhD, St. Louis, MO; adapted with permission.

Figure 2

A simplified model of the leptin signaling pathway. Central insulin can bind to the same neurons as leptin and is an anorexigenic signal. The ligands leptin, POMC, CART, and BDNF, the receptors for leptin, melanocortins, and BDNF, and the enzyme PC1 have been found to have function-altering mutations associated with obesity in children. Mutations in the ligands and receptors for NPY, AGRP, CPE, and MCH have been found to cause excessive weight gain when mutated in rodents, but have not been as convincingly shown to be associated with human obesity. OB-Rb, the signal-transducing form of the leptin receptor; NPY, neuropeptide Y; AGRP, agouti-related protein; POMC, pro-opiomelanocortin; CART, cocaine-amphetamine related transcript; PC 1, prohormone convertase 1; CPE, carboxypeptidase E; MSH, melanocyte stimulating hormone; NPYR, neuropeptide Y receptor; MC3R, melanocortin 3 receptor; MC4R, melanocortin 4 receptor; TRH, thyrotropin-releasing hormone; MCH, melanin concentrating hormone, GABA, gamma amino butyric acid; BDNF, brain-derived neurotrophic factor.

Figure 3

An algorithm for the work up of an obese child. Physical exam, growth patterns, and the child’s age should narrow the scope of the differential and dictate appropriate testing.