Exercise in obese female rats has beneficial effects on maternal and male and female offspring metabolism.

BACKGROUND: Maternal obesity (MO) impairs maternal and offspring health. Mechanisms and interventions to prevent adverse maternal and offspring outcomes need to be determined. Human studies are confounded by socio-economic status providing the rationale for controlled animal data on effects of maternal exercise (MEx) intervention on maternal (F0) and offspring (F1) outcomes in MO. HYPOTHESIS: MO produces metabolic and endocrine dysfunction, increases maternal and offspring glucocorticoid exposure, oxidative stress and adverse offspring outcomes by postnatal day (PND) 36. MEx in part prevents these outcomes. METHODS: F0 female rats ate either control or obesogenic diet from weaning through lactation. Half of each group wheel ran (from day 90 of life through pregnancy beginning day 120) providing four groups (n=8/group)--(i) controls, (ii) obese, (iii) exercised controls and (iv) exercised obese. After weaning, PND 21, F1 offspring ate a control diet. Metabolic parameters of F0 prepregnancy and end of lactation and F1 offspring at PND 36 were analyzed. RESULTS: Exercise did not change maternal weight. Before breeding, MO elevated F0 glucose, insulin, triglycerides, cholesterol, leptin, fat and oxidative stress. Exercise completely prevented the triglyceride rise and partially increases glucose, insulin, cholesterol and oxidative stress. MO decreased fertility, recovered by exercise. At the end of lactation, exercise returned all metabolic variables except leptin to control levels. Exercise partially prevented MO elevated corticosterone. F1 offspring weights were similar at birth. At PND 36, MO increased F1 male but not female offspring leptin, triglycerides and fat mass. In controls, exercise reduced male and female offspring glucose, prevented the offspring leptin increase and partially the triglyceride rise. CONCLUSIONS: MEx before and during pregnancy has beneficial effects on the maternal and offspring metabolism and endocrine function occurring with no weight change in mothers and offspring indicating the importance of body composition rather than weight in evaluations of metabolic status.

Maternal obesity and overnutrition increase oxidative stress in male rat offspring reproductive system and decrease fertility.

PURPOSE: Increasing evidence exists that maternal obesity (MO) and overnutrition during pregnancy and lactation have long-lasting consequences for progeny metabolism, cardiovascular and endocrine function. Data on effects of MO on offspring reproduction are limited. We hypothesized that MO during pregnancy and lactation in founder F(0) rat mothers would increase testicular and sperm oxidative stress (OS) and adversely impact male fertility in their F(1) offspring. METHODS: We induced pre-pregnancy MO by feeding F(0) females a high-fat diet from weaning through pregnancy and lactation. After weaning, all F(1) rats ate control (C) diet. We determined serum testosterone, malondialdehyde (MDA), reactive oxygen species (ROS) and superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity in F(1) testes and sperm at postnatal days (PNDs) 110, 450 and 650. RESULTS: At PNDs 450 and 650, MO offspring had lower luteinizing hormone while testosterone levels were lower at all ages. Testicular MDA and ROS concentrations and SOD and GPx activity were higher in MO F(1) at all ages. Nitrotyrosine immunostaining was higher at all ages in MO F(1) testes than C F(1). At PNDs 450 and 650, MO F(1) spermatozoa showed higher MDA concentrations and lower SOD and GPx activity with reduced sperm concentration, viability and motility, and more sperm abnormalities. Fertility rate was not affected at PND 110 but was lower in MO F(1) at PNDs 450 and 650. CONCLUSIONS: We conclude that MO during pregnancy and lactation increases F(1) testicular and sperm OS leading to premature aging of reproductive capacity.