TY - JOUR
T1 - Exercise in obese female rats has beneficial effects on maternal and male and female offspring metabolism
AU - Vega, C. C.
AU - Reyes-Castro, L. A.
AU - Bautista, C. J.
AU - Larrea, F.
AU - Nathanielsz, P. W.
AU - Zambrano, E.
N1 - Funding Information:
CCV is graduate student from posgrado de Ciencias Químico-Biológicas de la ENCB del Instituto Politécnico Nacional and is recipient of Consejo Nacional de Ciencias y Tecnología (CONACyT) fellowship. LARC and CJB are graduate students from Doctorado en Ciencias Biomédicas, Facultad de Medicina, Universidad Nacional Autónoma de México and are recipients of CONACyT fellowship; this work was supported by CONACyT 155166, México, Sociedad Mexicana de Nutrición y Endocrinología and HD 21350 from the National Institute of Child Health and Human Development.
PY - 2015/4/9
Y1 - 2015/4/9
N2 - 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.
AB - 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.
KW - exercise; programming
KW - maternal obesity
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U2 - 10.1038/ijo.2013.150
DO - 10.1038/ijo.2013.150
M3 - Article
C2 - 23949616
AN - SCOPUS:84927061964
SN - 0307-0565
VL - 39
SP - 712
EP - 719
JO - International Journal of Obesity
JF - International Journal of Obesity
IS - 4
ER -