Purpose of review: To describe our current understanding of the mechanisms involved in the regulation of linear growth in childhood obesity.
Recent findings: The developmental origins hypothesis has focused on low birth weight individuals with subsequent obesity, identifying a cascade of neuroendocrine regulatory factors involved in the progressive increase in body fat and metabolic risk. Yet, tall stature is the common clinical outcome of childhood obesity. Recent data have expanded our understanding of environmental influences on developing systems. Here, we review the elements of neuroendocrine systems contributing to the integration of metabolic controls involved in growth regulation in the obese child with particular emphasis on growth hormone, ghrelin, insulin-like growth factors and insulin.
Summary: Growth patterns of obesity during childhood are well described, documenting increased linear growth in early childhood associated with accelerated pubertal maturation resulting in normal adult height. Despite recent data suggesting that ghrelin and the growth hormone secretagogue receptor, as well as the insulin-like growth factors, their binding proteins and insulin have potential to be mediators of nutrient exposure and linear growth, it remains to be determined how these systems interrelate and determine growth. This is an area of ongoing investigation.