Reproductive processes (gametogenesis, hypothalamic-pituitary-gonadal function, and behavior) are masculinized or feminized during fetal development. At least some of these effects are determined during fetal development by androgens, estrogens, and glucocorticoids acting on cognate steroid receptors. These receptors, however, render reproductive development sensitive to endocrine-disrupting compounds that also act on the same receptors. Less well known is the fact that endocrine disruptors can alter energy balance (energy intake, storage, and expenditure). Recent evidence indicates that endocrine disruptors affect many individual processes known to contribute to obesity, including the gut microbiome, adipocyte differentiation, energy metabolism, ingestive behavior, and the tendency to accumulate adipose tissue in response to certain diets. Understanding effects of endocrine disruptors on energy balance will be aided by attention to the processes involved in sexual differentiation. This is because many energy-balancing traits are sexually dimorphic with the masculine phenotype most closely linked to metabolic diseases such as type II diabetes and heart disease. So far, it is clear that at least some endocrine disruptors have masculinizing effects via classical organizational effects on sexually dimorphic energy balancing traits during fetal development. In addition, we should expect endocrine disruptors to affect other defined mechanisms of sexual differentiation (e.g., sex chromosome action, aromatization, active feminization, and organizing actions at later periods of development, such as puberty). Investigators interested in effects of endocrine disruptors on peripheral metabolism often work in isolation from those interested in the effects of endocrine disruptors on ingestive behavior. In fact, changes in peripheral metabolism have organizational and activational effects on the neural circuitry that controls ingestive behavior. Together, these considerations demand a concerted multidisciplinary and integrative approach to the study of endocrine disruptors.