Pediatric Endocrine Disorders of Energy Balance

Abstract

The definition of obesity is a degree of somatic overweight that affords detrimental health consequences [1]. The majority of obesity in adulthood has its origins in childhood [2,3,4], making obesity a pediatric concern, and the prevention and treatment of obesity a pediatric goal. Weight gain obeys the First Rule of Thermodynamics, which states, “The total energy of the system plus the surroundings is constant”. Energy can neither be created nor destroyed, but can be transformed to matter and vice-versa. In human terms, “calories in = calories out + weight gain”. Obesity, in the simplest statement of pathophysiology, is a dysregulation of either increased energy intake or decreased energy expenditure or both to favor excessive weight gain [5]. Many lay “experts” consider obesity to be an aberrant behavior; the pathophysiologic result of gluttony and sloth. Within the scientific community, the discovery of leptin and the elucidation of various monogenic disorders of obesity and genetic linkages, has promulgated the notion that obesity is a disease. Instead, it is more correct to consider obesity as a phenotype of many different pathologic processes, which impact at various points on the negative feedback pathway of energy balance. Various processes can promote an obligate and primary weight gain, and that increased energy intake and decreased energy expenditure may secondarily result. Many of the defects in the negative feedback energy balance pathway result in an increased storage of energy in adipose tissue due to increased lipogenesis, decreased lipolysis, or both. This review will elucidate the genetic/endocrine disorders that promote weight gain and obesity in children.