Epidemiological studies initially demonstrated that maternal undernutrition leads to low birth weight with increased risk of adult-onset obesity. Maternal obesity and diabetes associated with high birth weight, excessive nutrition in neonates, and rapid catch-up growth also predispose offspring to fat accumulation. As stated by the Developmental Origin of Health and Disease concept, nutrient supply perturbations in the fetus or neonate result in long-term programming of individual body weight set-point. Adipose tissue is a key fuel storage unit mainly involved in the maintenance of energy homeostasis. Studies in numerous animal models have demonstrated that the adipose tissue is the focus of developmental programming events in a gender- and depot-specific manner. This review summarizes the impact of maternal nutritional manipulations on cellularity (i.e., cell number, size, and type) of adipose tissue in programmed offspring. In rodents, adipose tissue development is particularly active during the perinatal period, especially during the last week of gestation and during early postnatal life. In contrast to rodents, this process essentially takes place before birth in bigger mammals. Despite these different developmental time windows, altricial and precocial species share several mechanisms of adipose tissue programming. Maternal nutritional manipulations result in increased adipogenesis and modified fat distribution and composition. Inflammation changes such as infiltration of macrophages and increased inflammatory markers are also observed. Overall, it may predispose offspring to fat accumulation and obesity. Inappropriate hormone levels, modified tissue sensitivity, and epigenetic mechanisms are key factors involved in the programming of adipose tissue's cellularity during the perinatal period.