Allergenic activity of the native protein, explaining the allergenic potency of this protein. The obesity epidemic continues to worsen worldwide, with the most alarming increases occurring in children. If the current trends of childhood obesity continue, it is projected that 60 million children will be overweight or obese by 2020 worldwide. Obesity in children is not only becoming more prevalent, but is also beginning at younger ages, even as young as infants. Accelerated growth during infancy and perhaps even in utero programs not only increased susceptibility for obesity in later life, but also increases the risk of several obesity-related co-morbidities, such as insulin resistance and cardiovascular disease. This occurrence of early onset obesity suggests that the intrauterine environment may be contributing to the obesity epidemic through fetal programming of offspring metabolism and disruption of energy balance. Using a rat model of gestational obesity, we have previously shown that maternal obesity, at the time of conception, leads to greater fat mass, increased body fat percentage, and insulin resistance in the offspring in later life 130), and worsens when challenged with a high fat diet. Further, indications of metabolic abnormalities in these offspring are apparent as early as PND21 and include hepatic steatosis, mild hyperinsulinemia, and a lipogenic gene signature in the liver. It is possible that maternal obesity-induced exposure to elevated fatty acids in utero leads to a shunting of fatty acids towards lipogenesis and away from fatty acid oxidation. However, the precise mechanisms that contribute to increased susceptibility of offspring from obese dams to develop nonalcoholic fatty liver effect astrocytes dopaminergic neurons disease in early life, and obesity in later life, remain poorly understood. Hepatic mitochondria are of maternal origin, and as such, may be an important target to consider for investigating metabolic perturbations in offspring of obese women. Mitochondria are critical sites of metabolism and are associated with energy sensing. For example, mitochondrial dysfunction in the liver has been associated with the development of NAFLD in obese rats, as shown by: reduced fatty acid oxidation; decreased cytochrome c protein content in the liver ; and decreased carnitine palmitoyl-CoA transferase-1 activity. Moreover, maternal exposure to a high fat diet prior to conception, and during gestation and lactation, has been reported to lead to the development of NAFLD and insulin resistance in adult offspring that was linked to reduced mitochondrial electron transport chain activity in mice. Furthermore, mitochondrial dysfunction has been linked to human patients diagnosed with NAFLD. In the current study, we examined systemic and hepatic metabolic adaptations in offspring from lean and obese dams at PND21. First, we studied whether maternal obesity alters energy expenditure and substrate utilization in offspring using indirect calorimetry. Second, we sought to determine the role of mitochondrial function in offspring by measuring gene expression and protein content of key mitochondrial markers in the liver. Third, we investigated fasting-induced changes in hepatic mitochondrial markers involved in energy status. Our results demonstrate that offspring from obese rat dams have increased susceptibility to develop systemic and hepatic energy utilization perturbations that are mediated, in part, by mitochondrial dysfunction at weaning.