Neonatal Leptin Treatment Reverses Developmental Programming

• DOI: 10.1210/en.2005-0581
• Publication Date: 2005-07-15T00:14:08Z
• Authors: M. H. Vickers; P. D. Gluckman; A. H. Coveny; P. L. Hofman; W. S. Cutfield; A. Gertler; B. H. Breier; M. Harris
• Keywords: Hyperinsulinemia

An adverse prenatal environment may induce long-term metabolic consequences, in particular obesity and insulin resistance. Although the mechanisms are unclear, this programming has generally been considered an irreversible change developmental trajectory. Adult offspring of rats subjected to undernutrition during pregnancy develop obesity, hyperinsulinemia, hyperleptinemia, especially presence a high-fat diet. Reduced locomotor activity hyperphagia contribute increased fat mass. Using model maternal undernutrition, we investigated effects neonatal leptin treatment on phenotype adult female offspring. Leptin (rec-rat leptin, 2.5 μg/g·d, sc) from postnatal d 3–13 resulted transient slowing weight gain, particularly programmed offspring, normalized caloric intake, activity, body weight, mass, fasting plasma glucose, insulin, concentrations life contrast saline-treated undernourished mothers who developed all these features Neonatal had no demonstrable normally fed mothers. This study suggests that is potentially reversible by intervention late phase plasticity. The complete normalization implies reverse adaptations resulting relative fetal undernutrition.