Change in Calcium Balance and Bone Mineral Density during Pregnancy in Female Rats.

Omi, Naomi; Ezawa, Ikuko

doi:10.3177/jnsv.47.195

Cited by 5 publications

(3 citation statements)

References 14 publications

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“…In the present studies, pregnancy itself did not alter BMD or BMC. These data are consistent with reports of increased calcium absorption in pregnant rats and most of the calcium and phosphorous demands of the pregnant dams being supplied from the diet (41,42). Furthermore, the diets given using the TEN system have been shown to be better than rodent chow diets in maintaining skeletal integrity (43).…”

Section: Discussionsupporting

confidence: 91%

Different Molecular Mechanisms Underlie Ethanol-Induced Bone Loss in Cycling and Pregnant Rats

et al. 2006

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Chronic ethanol (EtOH) consumption can result in osteopenia. In the current study, we examined the modulation of EtOH-induced bone loss during pregnancy. Nonpregnant and pregnant dams were intragastrically infused either control or EtOH-containing diets throughout gestation (gestation d 5 through 20 or an equivalent period of 15 d) by total enteral nutrition. The effects of EtOH (8.5 to 14 g/kg/d) on tibial bone mineral density (BMD), mineral content (BMC), and bone mineral area were assessed at gestation d 20 via peripheral quantitative computerized tomography. EtOH caused a dose-dependent decrease in BMD and BMC without affecting bone mineral area. Trabecular BMD and BMC were significantly lower in EtOH-treated, nonpregnant dams, compared with pregnant cohorts at the same infused dose of EtOH and urinary ethanol concentrations. Static histomorphometric analysis of tibiae from pregnant rats after EtOH treatment showed decreased osteoblast and osteoid surface, indicating inhibited bone formation, whereas EtOH-treated cycling rats showed higher osteoclast and eroded surface, indicative of increased bone resorption. Circulating osteocalcin and 1,25-dihydroxyvitamin D3 were lower in both EtOH-fed nonpregnant and pregnant rats. Gene expression of osteoclast markers, 70 kDa v-ATPase, and tartrate-resistant acid phosphatase were increased selectively in nonpregnant EtOH-treated rats but not pregnant rats. Moreover, only nonpregnant EtOH-fed rats showed induction in bone marrow receptor activator of nuclear factor-kappaB ligand mRNA and decreased circulating 17beta-estradiol levels. Our data suggest that EtOH-induced bone loss in pregnant rats is mainly due to inhibited bone formation, whereas in nonpregnant rats, the data are consistent with increased osteoclast activation and bone resorption concomitant with decreased estradiol levels.

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Section: Discussionsupporting

confidence: 91%

Different Molecular Mechanisms Underlie Ethanol-Induced Bone Loss in Cycling and Pregnant Rats

et al. 2006

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“…During pregnancy, females increase their absorption of calcium in the alimentary tract (Halloran & DeLuca 1980). Although urinary losses also increase (Omi & Ezawa 2001), the elevated absorption leads to elevated calcium levels in the blood (hypercalciuria), which persist throughout reproduction (Sarli et al 2005). In the first trimester of pregnancy, this extra uptake may actually exceed the foetal growth requirements.…”

Section: Indirect Costs (A) Optional Compensatory Costs (I) Thermoregmentioning

confidence: 99%

“…In the first trimester of pregnancy, this extra uptake may actually exceed the foetal growth requirements. Consequently, there is a phase of bone accretion in the earliest part of pregnancy (Zeni et al 1999;Omi & Ezawa 2001), which is characterized by increases in markers of bone turnover (like osteocalcin and alkaline phosphatase levels; Sengupta et al 2005). This bone accretion appears to act as a temporary storage of calcium that can be withdrawn as the pregnancy proceeds and the foetal demands for calcium increase.…”

Section: Indirect Costs (A) Optional Compensatory Costs (I) Thermoregulatory Demandsmentioning

confidence: 99%

The physiological costs of reproduction in small mammals

Speakman

2007

Phil. Trans. R. Soc. B

633

694

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Life-history trade-offs between components of fitness arise because reproduction entails both gains and costs. Costs of reproduction can be divided into ecological and physiological costs. The latter have been rarely studied yet are probably a dominant component of the effect. A deeper understanding of life-history evolution will only come about once these physiological costs are better understood. Physiological costs may be direct or indirect. Direct costs include the energy and nutrient demands of the reproductive event, and the morphological changes that are necessary to facilitate achieving these demands. Indirect costs may be optional 'compensatory costs' whereby the animal chooses to reduce investment in some other aspect of its physiology to maximize the input of resource to reproduction. Such costs may be distinguished from consequential costs that are an inescapable consequence of the reproductive event. In small mammals, the direct costs of reproduction involve increased energy, protein and calcium demands during pregnancy, but most particularly during lactation. Organ remodelling is necessary to achieve the high demands of lactation and involves growth of the alimentary tract and associated organs such as the liver and pancreas. Compensatory indirect costs include reductions in thermogenesis, immune function and physical activity. Obligatory consequential costs include hyperthermia, bone loss, disruption of sleep patterns and oxidative stress. This is unlikely to be a complete list. Our knowledge of these physiological costs is currently at best described as rudimentary. For some, we do not even know whether they are compensatory or obligatory. For almost all of them, we have no idea of exact mechanisms or how these costs translate into fitness trade-offs.

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