Adipocytes as Target Cells for Endocrine Disruption

E. Diamanti-Kandarakis and A.C. Gore (eds.), Endocrine Disruptors and Puberty, Contemporary Endocrinology, DOI 10.1007/978-1-60761-561-3_10, © Springer Science+Business Media, LLC 2012 Abstract Throughout the fi rst two decades of human development, growth of adipose tissue primarily results from an increase in adipocyte number (hyperplasia). Once established, the number of fat cells remains relatively constant, and adipose tissue grows larger primarily by fi lling the resident cells with more fat (hypertrophy). Obese children exhibit an augmented rate of increase in adipocyte number, and correspondingly, obese adults possess more fat cells. Hence, childhood and adolescence appear to be critical periods in establishing the number of fat cells. Endocrine-disrupting chemicals (EDCs) can predispose a child to obesity by infl uencing all aspects of adipose tissue growth, starting from multipotent stromal cells (MSCs) and ending with mature adipocytes. EDC exposure can increase the number of preadipocytes, enhance the differentiation of preadipocytes into adipocytes, and augment the uptake of fat into existing adipocytes. Unlike genetic mechanisms, which require a mutation event, EDCs have the capacity to quantitatively alter gene expression by modulating cellular-signaling pathways and by introducing epigenetic changes that also alter gene expression. Therefore, EDC exposure could foster a swift change in the metabolic profi le of a population, which might provide at least a partial explanation for the rapid rise in obesity. This review focuses on the developmental origins of the adipocyte and its connection to early-onset obesity with the aim of providing a foundation for formulating hypotheses regarding how EDCs can interfere with adipogenesis and contribute to the obesity epidemic.