Vega C C, Reyes-Castro L A, Bautista C J, Larrea F, Nathanielsz P W, Zambrano E
1] Department of Reproductive Biology, National Institute of Medical Science and Nutrition Salvador Zubirán, Mexico City, Mexico [2] Biological Science School, Polytechnic National Institute, Mexico City, Mexico.
Department of Reproductive Biology, National Institute of Medical Science and Nutrition Salvador Zubirán, Mexico City, Mexico.
Int J Obes (Lond). 2015 Apr;39(4):712-9. doi: 10.1038/ijo.2013.150. Epub 2013 Aug 16.
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.
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.
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.
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.
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.
母亲肥胖（MO）会损害母亲和后代的健康。需要确定预防不良母婴结局的机制和干预措施。人类研究因社会经济地位而受到混淆，这为关于母亲运动（MEx）干预对MO母亲（F0）和后代（F1）结局影响的对照动物数据提供了理论依据。
MO会导致代谢和内分泌功能障碍，在出生后第36天增加母亲和后代的糖皮质激素暴露、氧化应激以及不良后代结局。MEx部分预防这些结局。
F0雌性大鼠从断奶到哺乳期食用对照饮食或致肥胖饮食。每组中的一半进行轮转跑步（从生命第90天到怀孕第120天开始），从而形成四组（每组n = 8）——（i）对照组，（ii）肥胖组，（iii）运动对照组和（iv）运动肥胖组。断奶后，在出生后第21天，F1后代食用对照饮食。分析F0孕前和哺乳期结束时以及出生后第36天F1后代的代谢参数。
运动未改变母亲体重。在繁殖前，MO升高了F0的血糖、胰岛素、甘油三酯、胆固醇、瘦素、脂肪和氧化应激。运动完全阻止了甘油三酯的升高，并部分增加了血糖、胰岛素、胆固醇和氧化应激。MO降低了生育能力，运动可使其恢复。在哺乳期结束时，运动使除瘦素外的所有代谢变量恢复到对照水平。运动部分预防了MO引起的皮质酮升高。F1后代出生时体重相似。在出生后第36天，MO增加了F1雄性而非雌性后代的瘦素、甘油三酯和脂肪量。在对照组中，运动降低了雄性和雌性后代的血糖，阻止了后代瘦素的增加，并部分阻止了甘油三酯的升高。
孕期及孕前的MEx对母亲和后代的代谢及内分泌功能有有益影响，母亲和后代体重无变化，这表明在评估代谢状态时身体成分而非体重的重要性。
