Physiological skeletal gains and losses in rat mothers during pregnancy and lactation are not observed following uteroplacental insufficiency

2014 ◽  
Vol 26 (3) ◽  
pp. 385 ◽  
Author(s):  
Tania Romano ◽  
John D. Wark ◽  
Mary E. Wlodek

Fluctuations in maternal bone mass during pregnancy and lactation facilitate calcium transfer to offspring. Uteroplacental insufficiency causes fetal growth restriction and programs poor adult bone health. We aimed to characterise maternal skeletal phenotype during normal pregnancy and pregnancy complicated by uteroplacental insufficiency. Uteroplacental restriction (Restricted) or sham surgery (Control) was performed on gestational Day 18 (term = 22 days) in pregnant Wistar-Kyoto rats. Maternal right femurs were collected on embryonic Day 20, postnatal Day 1 and Weeks 5, 7 and 9 postnatal. Dual-energy X-ray absorptiometry was used to quantify global bone mineral content, density and body composition. Peripheral quantitative computed tomography was utilised to determine trabecular and cortical content, density, circumferences and strength. Control rats exhibited expected reductions in trabecular and cortical content, density and bone strength from embryonic Day 20 to postnatal Day 1 (P < 0.05). These skeletal alterations were absent in Restricted rats. By postnatal Day 7, bone parameters in Control and Restricted rats were not different from non-pregnant rats, indicating restoration of maternal bone. The lack of bone loss in mothers suffering uteroplacental insufficiency suggests that calcium transfer to pups would be impaired. This reduction in calcium availability is a likely contributor to the programming of poor adult bone health in growth-restricted offspring.

2018 ◽  
Vol 314 (2) ◽  
pp. R161-R170 ◽  
Author(s):  
Kristina Anevska ◽  
Jean N. Cheong ◽  
John D. Wark ◽  
Mary E. Wlodek ◽  
Tania Romano

Females born growth restricted have poor adult bone health. Stress exposure during pregnancy increases risk of pregnancy complications. We determined whether maternal stress exposure in growth-restricted females exacerbates long-term maternal and offspring bone phenotypes. On gestational day 18, bilateral uterine vessel ligation (restricted) or sham (control) surgery was performed on Wistar-Kyoto rats. At 4 mo, control and restricted females were mated and allocated to unstressed or stressed pregnancies. Stressed pregnancies had physiological measurements performed; unstressed females were not handled. After birth, mothers were aged to 13 mo. Second-generation (F2) offspring generated four experimental groups: control unstressed, restricted unstressed, control stressed and restricted stressed. F2 offspring were studied at postnatal day 35 (PN35), 6, 12, and 16 mo. Peripheral quantitative computed tomography was performed on maternal and F2 offspring femurs. Restricted females, irrespective of stress during pregnancy, had decreased endosteal circumference, bending strength, and increased osteocalcin concentrations after pregnancy at 13 mo. F2 offspring of stressed mothers were born lighter. F2 male offspring from stressed pregnancies had decreased trabecular content at 6 mo and decreased endosteal circumference at 16 mo. F2 female offspring from growth-restricted mothers had reduced cortical thickness at PN35 and reduced endosteal circumference at 6 mo. At 12 mo, females from unstressed restricted and stressed control mothers had decreased trabecular content. Low birth weight females had long-term bone changes, highlighting programming effects on bone health. Stress during pregnancy did not exacerbate these programmed effects. Male and female offspring responded differently to maternal growth restriction and stress, indicating gender-specific programming effects.


Nutrients ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1236
Author(s):  
Kristina Anevska ◽  
Dayana Mahizir ◽  
Jessica F. Briffa ◽  
Andrew J. Jefferies ◽  
John D. Wark ◽  
...  

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.


2020 ◽  
Vol 50 (12) ◽  
pp. 1781-1787
Author(s):  
David J. Fennimore ◽  
Maria Digby ◽  
Margaret Paggiosi ◽  
Paul Arundel ◽  
Nick J. Bishop ◽  
...  

Abstract Bone health in children with osteogenesis imperfecta is monitored using radiographs and dual-energy X-ray absorptiometry, which have limitations. High-resolution peripheral quantitative CT can non-invasively derive bone microarchitectural data. Children with severe osteogenesis imperfecta have fragile deformed bones, and positioning for this scan can be difficult. We assessed the feasibility of high-resolution peripheral quantitative CT in nine children aged 9–15 years with osteogenesis imperfecta and compared results with dual-energy X-ray absorptiometry and with healthy controls. All nine recruited children were successfully scanned and showed no preference for either modality. It therefore appears feasible to perform high-resolution peripheral quantitative CT in children with osteogenesis imperfecta aged 9 years and older. Future studies should focus on understanding the clinical implications of the technology in this patient cohort.


Author(s):  
Ronald Barr ◽  
Dean Inglis ◽  
Uma Athale ◽  
Maciej Jaworski ◽  
Troy Farncombe ◽  
...  

Background – Loss of bone mineral is a common concomitant of the treatment of acute lymphoblastic leukemia (ALL) due mainly to chemotherapy, especially with corticosteroids. Osteopenia/osteoporosis may persist long into survivorship. Measurement of bone mineral density (BMD) by dual energy X-ray absorptiometry is limited to two-dimensionality and cannot distinguish trabecular from cortical bone. Methods – A sample of 74 subjects, more than 10 years from diagnosis, underwent peripheral quantitative computed tomography (pQCT) at metaphyseal (trabecular bone) and diaphyseal (cortical bone) sites in the radius and tibia. pQCT provides three-dimensional assessment of bone geometry, density and architecture. Results – Similarities of average values in multiple metrics with those in healthy subjects obscured deficits in both trabecular and cortical bone, as well as bone strength, revealed by Z scores using an ethnically comparable sample of healthy individuals. Connectivity, a measure of bone architecture and a surrogate measure of bone strength, was lower in females than males. Survivors of standard risk ALL had greater connectivity in and more compact trabecular bone than high risk survivors who had received more intensive osteotoxic chemotherapy. There were no statistically significant differences in any of the metrics at any of the sites between subjects who had or had not a history of fracture, cranial irradiation or use of a bisphosphonate. Conclusions – These long-term survivors of ALL have somehat compromised bone health, but data in comparable healthy populations are limited. Longitudinal studies in larger and more ethnically diverse cohorts will provide greater insight into bone health in this vulnerable population.


1987 ◽  
Vol 58 (3) ◽  
pp. 415-425 ◽  
Author(s):  
Jean-Marc Dollet ◽  
Bernard Beck ◽  
Jean-Pierre Max ◽  
Gérard Debry

1. In developing countries, malnutrition begins during pregnancy and lactation. Glucose intolerance is a problem of importance during protein-energy malnutrition (PEM). We therefore studied glucose homeostasis in rats weaned from undernourished mothers.2. On weaning, 156 mde Wistar rats, born from deprived mothers (75 g casein/kg diet), were fed ad lib on either a balanced diet (180 g casein/kg; group DR), or a protein-deficient diet (50 g casein/kg; group DD). At seven time intervals (weeks 0, 1, 3, 5, 8, 16 and 23) twelve rats were weighed, fasted overnight and then decapitated. Blood glucose, plasma insulin (IRI) and glucagon (IRG) levels and pancreatic insulin and glucagon contents were determined.3. In DR and DD rats blood glucose, which was normal at weaning, dropped in the 1st week and then increased slowly. DR rats were hyperglycaemic from week 16. IRI continually increased during the experiment from near-normal values to hyperinsulinic levels in DR rats; in group DD, it remained stable until week 8 before increasing. IRG, which was very low at weaning, increased to normal levels in the 1st week in group DR; in group DD, it fell slightly during the study. Pancreatic hormone contents were much higher than after normal pregnancy and lactation.4. We compared these results with those of a previous study with rats born from normal mothers: at weaning in the second experiment the rats were already well adapted to malnutrition. The plasma ratio IRI:IRG in DD rats showed two phases of adaptation: weeks 0–5 when glucose homeostasis did not change and weeks 5–23 when it became increasingly normal. At the end of the experiment DR rats still had a lower body-weight than normal rats but were insulin-resistant.


2013 ◽  
Vol 22 (01) ◽  
pp. 13-17
Author(s):  
J. M. Patsch ◽  
R. Kocijan ◽  
H. Resch ◽  
J. Haschka

ZusammenfassungKnochenstabilität ist durch Knochenvolumen und Mikroarchitektur des Knochens determiniert. Mittels HR-pQCT (high resolution peripheral quantitative computed tomography) steht eine nicht invasive Methode zur Verfügung, um die Mikroarchitektur des Knochens darzustellen. Die Resultate aus zahlreichen Studien geben Rückschlüsse auf unterschiedliche Strukturalterationen im Rahmen von Erkrankungen, die mit einem erhöhten Frakturrisiko einhergehen. Die Knochendichtemessung mittels DXA spiegelt das Frakturrisiko oft nicht adäquat wider. Umso entscheidender ist es, Risikofaktoren in der Wahl der Therapie zu berücksichtigen. Die klinische Relevanz der Resultate aus HR-pQCT-Messungen besteht derzeit dahingehend, dass wertvolle Informationen über Veränderungen der Mikroarchitektur auf Forschungsebene erhoben werden.


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