Effect of Diabetes Mellitus on Maternofetal Flux of Calcium and Magnesium and Calbindin9K mRNA Expression in Rat Placenta

Husain, Shahid; Birdsey, T. J.; Glazier, Jocelyn D.; Mughal, M Z; Garland, Hugh; Sibley, Colin P.

doi:10.1203/00006450-199403000-00022

Cited by 47 publications

(36 citation statements)

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“…1 ]. These data demonstrate that the fetomaternal calcium gradient in these mice is established between E17 and E19, and further suggest that active transplacental calciumtransport mechanisms during this period begin to contribute significantly to maternofetal calcium flux, consistent with other studies in mice and rats (23)(24)(25)(26). In contrast, fetal blood [Ca 2+ ] in P0 was significantly lower than WT and maternal blood at both E17 and E19 (P < 0.05).…”

Section: Resultssupporting

confidence: 67%

“…However, by E19 calbindin-D 9K expression was comparable between the two genotypes. This mirroring of the trend observed in the fetal calcium content of P0 fetuses and the placental expression of calbindin-D 9K over days E17 to E19 lends further support for the concept that calbindin-D 9K expression is rate-limiting for fetal calcium acquisition in rodents (23,24,30,31).…”

Section: Resultsmentioning

confidence: 55%

“…However, at E17 we found that 45Ca K mf was not different between P0 and WT fetuses, although calbindin-D 9K expression was significantly reduced in the placentas of P0 fetuses, entirely consistent with their reduced fetal calcium content. This discordance between placental calbindin-D 9K expression and maternofetal calcium flux was surprising in the light of other evidence showing a good correspondence between these variables under different situations (23,24,30). This finding could relate to the gestational timing of our observations, as there is a highly exponential gestational increase in Ca J mf between E17 and E19 in rodents (23,30 bearing in mind that fetal skeletal mineralization occurs over the last few days of gestation in rodents and placental calbindin-D 9K expression is comparatively low before E15 (30,(33)(34)(35)(36).…”

Section: Resultsmentioning

confidence: 99%

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Placental-specific Igf2 knockout mice exhibit hypocalcemia and adaptive changes in placental calcium transport

Dilworth¹,

Kusinski²,

Cowley³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Evidence is emerging that the ability of the placenta to supply nutrients to the developing fetus adapts according to fetal demand. To examine this adaptation further, we tested the hypothesis that placental maternofetal transport of calcium adapts according to fetal calcium requirements. We used a mouse model of fetal growth restriction, the placental-specific Igf2 knockout (P0) mouse, shown previously to transiently adapt placental System-A amino acid transporter activity relative to fetal growth. Fetal and placental weights in P0 mice were reduced when compared with WT at both embryonic day 17 (E17) and E19. Ionized calcium concentration [Ca 2+ ] was significantly lower in P0 fetal blood compared with both WT and maternal blood at E17 and E19, reflecting a reversal of the fetomaternal [Ca 2+ ] gradient. Fetal calcium content was reduced in P0 mice at E17 but not at E19. Unidirectional maternofetal calcium clearance ( Ca K mf ) was not different between WT and P0 at E17 but increased in P0 at E19. Expression of the intracellular calcium-binding protein calbindin-D 9K , previously shown to be rate-limiting for calcium transport, was increased in P0 relative to WT placentas between E17 and E19. These data show an increased placental transport of calcium from E17 to E19 in P0 compared to WT. We suggest that this is an adaptation in response to the reduced fetal calcium accumulation earlier in gestation and speculate that the ability of the placenta to adapt its supply capacity according to fetal demand may stretch across other essential nutrients.fetal growth restriction | calbindin | PMCA | pregnancy

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Section: Resultssupporting

confidence: 67%

Section: Resultsmentioning

confidence: 55%

Section: Resultsmentioning

confidence: 99%

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Placental-specific Igf2 knockout mice exhibit hypocalcemia and adaptive changes in placental calcium transport

Dilworth¹,

Kusinski²,

Cowley³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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“…We have previously shown that unidirectional calcium transport across the placenta of the diabetic pregnant rat is impaired [29] and that OD fetuses in utero are calcium deficient [29]. This could exacerbate the glucose effect described above, fetal calcium deficiency resulting in decreased tubular concentrations of calcium and, in turn, the upregulation of the calcium-transporting proteins.…”

Section: Discussionmentioning

confidence: 97%

Diabetes in rat pregnancy alters renal calcium and magnesium reabsorption and bone formation in adult offspring

et al. 2005

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Aims/hypothesis: We tested the hypothesis that diabetes in pregnancy can result in the in-utero reprogramming of renal calcium and magnesium handling and of bone formation in the offspring, which persists into adulthood. Methods: Male offspring of streptozotocintreated diabetic rats (OD rats) and of control non-diabetic animals (OC rats) were investigated as neonates and at 8, 12 and 16 weeks of age. Results: Compared with OC rats, urinary calcium and magnesium output was significantly reduced in OD rats at every age studied; Na + and K + outputs were unaffected. The renal expression of proteins involved in the tubular reabsorption of calcium (calcium ATPase, calbindin-D 28k and epithelial calcium channel) was increased in OD animals compared with that in OC animals. Additionally, we observed that adult OD rats had lower trabecular and higher cortical femoral bone volumes, explained by deposition of bone on the endosteal surface. Conclusions/interpretation: These data show that diabetes in pregnancy has profound effects on male offspring in terms of renal tubular calcium and magnesium reabsorption and the normal pattern of bone formation. These effects persist into adulthood. Such long-lasting effects of diabetes on kidney and the skeleton were not suspected and could have important implications for the health of children born to diabetic women.

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“…The mechanism for the lower bone SOS in LGA infants is not clear. When maternal diabetes coexists, decreased maternal mineral stores, 12,13 and decreased placental mineral transport 14 have been suggested as contributing factors. The very perturbed maternal -fetal environment in diabetes may be influential by many other potential mechanisms.…”

Section: Littner Et Almentioning

confidence: 99%

Decreased Bone Ultrasound Velocity in Large-for-Gestational-Age Infants

et al. 2003

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BACKGROUND:Bone speed of sound is a measure of bone breakability. There are few reports on bone mineral content in large for gestational age infants; most of them in infants of diabetic mothers. There are no data on bone speed of sound in large for gestational age infants of nondiabetic mothers. OBJECTIVE:To test the hypothesis that large for gestational age infants of nondiabetic mothers have lower bone speed of sound than appropriate for gestational age infants. DESIGN/METHODS:Bone speed of sound was measured within the first 96 hours of life at the right tibial midshaft in 25 singleton large for gestational age infants of non diabetic mothers and compared to appropriate for gestational age controls. RESULTS:Bone speed of sound measured in large for gestational age infants of nondiabetic mothers was lower than in controls.CONCLUSIONS: Large for gestational age infants of nondiabetic mothers have lower bone speed of sound than controls.

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Effect of Diabetes Mellitus on Maternofetal Flux of Calcium and Magnesium and Calbindin9K mRNA Expression in Rat Placenta

Cited by 47 publications

References 4 publications

Placental-specific Igf2 knockout mice exhibit hypocalcemia and adaptive changes in placental calcium transport

Placental-specific Igf2 knockout mice exhibit hypocalcemia and adaptive changes in placental calcium transport

Diabetes in rat pregnancy alters renal calcium and magnesium reabsorption and bone formation in adult offspring

Decreased Bone Ultrasound Velocity in Large-for-Gestational-Age Infants

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