Exposure to nicotine at a low dose during gestation might stimulate proliferation, differentiation, neurite outgrowth, and synaptogenesis of developing hypothalamic POMC neurons, thereby sensitizing leptin-melanocortinergic signaling in adult offspring, whereas exposure to nicotine at a high dose during gestation and lactation might impair those processes, leading to the reported obesity and diabetes phenotypes in adult offspring. The gene discussed is POMC; the disease is obesity due to melanocortin 4 receptor deficiency.