Neonatal stress induces insulin resistance, obesity and diabetes in adult male mice

Neonatal Stress Induces Insulin Resistance, Obesity and Diabetes in Adult Male Mice Many studies in men and in ani Many studies in men and in animals have shown that poor growth in fetal and postnatal life is associated to an increased risk for obesity, type 2 diabetes and metabolic syndrome in adult life. Maturation of pancreatic islets occurs in late pregnancy and in neonatal period and may be influenced by metabolic, endocrine and nervous stimuli. We investigated in mice the effect of psychological and nociceptive stimuli during neonatal period on endocrine and metabolic status in adult life. Litters (males) were randomly assigned to control and to manipulated group (sterile saline s.c. injection 1 ml/Kg during mother deprivation for 10 min. along 21 days ). Body weight, daily food and water intake, locomotor activity were measured at regular intervals. The caloric efficiency was calculated as grams of body weight gained divided grams of food ingested. At 120 days trunk body samples were collected and glucose, lipids, insulin and leptin were measured. [br]Body weight in manipulated mice was significantly higher at 60 days and thereafter: g. 52.5 1.3 vs g. 61.8 0.9 final weight, the same was for the epidydimal fat pads: g. 2.5 0.2 vs g. 1.2 0.3. The caloric efficiency was significantly higher in manipulated mice: 0.025 0.003 vs 0.012 0.001. No difference in food and water intake and spontaneous motor activity. Our data show that mild nociceptive stimuli early in life may induce, in non genetically prone mice, a condition of insulin resistance with obesity and diabetes.