Abstract
Growth restriction programs adult bone deficits and increases the risk of obesity, which may be exacerbated during pregnancy. We aimed to determine if high-fat feeding could exacerbate the bone deficits in pregnant growth restricted dams, and whether treadmill exercise would attenuate these deficits. Uteroplacental insufficiency was induced on embryonic day 18 (E18) in Wistar Kyoto (WKY) rats using bilateral uterine vessel ligation (restricted) or sham (control) surgery. The F1 females consumed a standard or high-fat (HFD) diet from 5 weeks, commenced treadmill exercise at 16 weeks, and they were mated at 20 weeks. Femora and plasma from the pregnant dams were collected at post-mortem (E20) for peripheral quantitative computed tomography (pQCT), mechanical testing, histomorphometry, and plasma analysis. Sedentary restricted females had bone deficits compared to the controls, irrespective of diet, where such deficits were prevented with exercise. Osteocalcin increased in the sedentary restricted females compared to the control females. In the sedentary HFD females, osteocalcin was reduced and CTX-1 was increased, with increased peak force and bending stress compared to the chow females. Exercise that was initiated before and continued during pregnancy prevented bone deficits in the dams born growth restricted, whereas a HFD consumption had minimal bone effects. These findings further highlight the beneficial effects of exercise for individuals at risk of bone deficits.
Highlights
Pregnancy is associated with changes in the maternal skeleton to meet the needs of the developing fetal skeleton [1,2]
In the exercise cohort, the HFD fed females were heavier at 15 weeks, 19 weeks, mating, throughout pregnancy (Table 2), and post-mortem (p < 0.05, Table 2)
This study demonstrates, for the first time that the bone deficits in sedentary restricted females were prevented with exercise, which was independent of the changes in osteocalcin and CTX-1 concentrations; suggesting that bone formation and resorption remain coupled
Summary
Pregnancy is associated with changes in the maternal skeleton to meet the needs of the developing fetal skeleton [1,2]. Our rat model of uteroplacental insufficiency, induced by bilateral uterine vessel ligation late in gestation to reduce fetal oxygen and nutrient transfer, mimics the 10–15% reduction in birth weight observed in humans [14,18,19], and it programs poor bone health in F0 dams and their F1 offspring. We have reported that F1 growth restricted females have normal skeletal adaptations during late gestation, with their F2 offspring having normal bone health [18]. This highlights that the programmed bone effects of growth restriction only influence the F1 generation
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