Calcium metabolism in diabetic mother, fetus, and newborn infant

Cruikshank, D. P.; Pitkin, Roy M.; Varner, Michael W.; Williams, George C.; Hargis, G. K.

doi:10.1016/0002-9378(83)90858-x

Cited by 34 publications

(26 citation statements)

References 15 publications

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“…Calcitonin The lack of differences in calcitonin concentrations between our three groups throughout gestation compares well with previous human data for calcitonin (Cruickshank et al 1980(Cruickshank et al , 1983. Thus it seems unlikely that calcitonin affects calbindin-D expression in the placenta or kidney.…”

Section: 25(oh) 2 Dsupporting

confidence: 88%

“…One study has reported lower PTH concentrations in DP than in CP rats (Verhaeghe et al 1999). However, clinical studies have found similar (Cruickshank et al 1980, Mimouni et al 1989 or reduced (Cruickshank et al 1983) serum PTH concentrations in diabetic pregnant women compared with controls. In the non-pregnant diabetic rat, PTH concentrations have been found to be slightly lower than those in controls (Takeshita et al 1994), which agrees with the early gestational measures in our study.…”

Section: 25(oh) 2 Dmentioning

confidence: 83%

See 1 more Smart Citation

Altered calbindin mRNA expression and calcium regulating hormones in rat diabetic pregnancy

Hamilton¹,

Tein²,

Glazier³

et al. 2000

Journal of Endocrinology

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Offspring of rats with diabetes mellitus are at risk of reduced calcium and bone mineral content. Altered expression of the maternal calcium binding proteins, calbindin-D 9K and calbindin-D 28K , which are involved in renal and placental calcium transport, may underlie these problems.We have investigated the effect of diabetes on circulating concentrations of regulatory hormones with respect to calbindin-D mRNA concentrations. Three rat groups were studied; control (CP), streptozotocininduced diabetic (DP), and insulin-treated diabetic (DPI) pregnant rats. Calbindin-D 9K and calbindin-D 28K mRNA abundance in placenta and maternal kidney were measured at days 7, 15, 18 and 21 of gestation, together with serum or plasma concentrations of 1,25 dihydroxyvitamin D 3 (1,25(OH) 2 D 3 ), parathyroid hormone (PTH), PTH-related protein (PTHrP), calcitonin, oestradiol and IGF-I. An increase in placental calbindin-D 9K mRNA abundance between days 18 and 21 in CP and DPI rats was severely blunted in the DP rats. In contrast, renal calbindin-D 28K mRNA abundance was greater at days 7, 15 and 18 in DP compared with CP rats, as was calbindin-D 9K at day 18. Calcitonin concentrations showed no differences between the groups, and both PTH and IGF-I were reduced over the first half of gestation, unlike the calbindins. In contrast, the concentrations of PTHrP and 1,25(OH) 2 D 3 were reduced at term in the DP group compared with the other two groups. Plasma oestradiol concentrations were lower in DP than in CP rats at days 7, 15 and 18, and most striking was the absence in DP rats of the peak of oestradiol seen at day 18 in CP rats. Despite the similarity between changes in placental calbindin mRNA and 1,25(OH) 2 D 3 , previous work has shown placental calbindin-D 9K regulation to be vitamin-D-independent. These studies produce suggestive evidence, therefore, that PTHrP and oestradiol may be involved in the altered calbindin-D expression by kidney and placenta in rat diabetic pregnancy.

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Section: 25(oh) 2 Dsupporting

confidence: 88%

Section: 25(oh) 2 Dmentioning

confidence: 83%

Altered calbindin mRNA expression and calcium regulating hormones in rat diabetic pregnancy

Hamilton¹,

Tein²,

Glazier³

et al. 2000

Journal of Endocrinology

View full text Add to dashboard Cite

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“…[6][7][8][9] Even the infants of maternal gestational DM are known decreased bone strength. 20 The decreased bone mineral content could be due to the increased bone resorption.…”

Section: Discussionmentioning

confidence: 99%

“…4 Furthermore, infants of the diabetic mother are known to have deceased mineral content. [6][7][8][9] Animal models have shown that diabetes in pregnancy associated with skeletal complications such as delayed fetal skeletal ossification. 10,11 There is a lack of experimental evidence weather the reduced bone mineral content associated with reduced skeletal growth in the diabetic infants.…”

Section: Introductionmentioning

confidence: 99%

Effect of <i>Cissus quadrangularis</i> Linn on skeletal growth in the neonates of diabetic rats

Sirasanagandla

Pai

Bhat

2014

Int J Basic Clin Pharmacol

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“…In addition, hypocalcemia and reduced bone mineral content are found in neonates of diabetic mothers (3,(5)(6)(7). However, some of the methodology used in earlier studies of neonatal bone mineral content has been questioned in a report that found no changes caused by maternal diabetes (8).…”

mentioning

confidence: 99%

Gamma-Linoleic Acid and Ascorbate Improves Skeletal Ossification in Offspring of Diabetic Rats

et al. 2002

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Maternal diabetes causes a range of complications in offspring, including reduced skeletal ossification. This study examined whether feeding ␥-linoleic acid (GLA) and ascorbate, alone or in combination, to diabetic pregnant rats improves skeletal development in their offspring. In addition, Ca 2ϩ concentration was monitored in maternal plasma and fetal tissue, as well as placental mRNA expression of calbindin-D 9k . Female rats rendered diabetic with streptozotocin were fed GLA (500 mg/kg/d), ascorbate (290 mg/kg/d), ascorbyl-GLA (790 mg/kg/d), or GLA and ascorbate (500 and 290 mg/kg/d, respectively) throughout pregnancy. Fetal skeletons were studied after alizarin red staining. Fewer ossification centers were observed in offspring of diabetic rats compared with offspring of control rats (68 Ϯ 4% of control, p ϭ 0.01). An almost complete restoration of ossification occurred with all the treatments (92-95 Ϯ 3% of control). Maternal diabetes during pregnancy is associated with an increased risk of several complications in the offspring, such as altered fetal growth, polyhydramnios, fetal loss, and congenital malformations (1-4). In addition, hypocalcemia and reduced bone mineral content are found in neonates of diabetic mothers (3, 5-7). However, some of the methodology used in earlier studies of neonatal bone mineral content has been questioned in a report that found no changes caused by maternal diabetes (8).Several potential mechanisms have been proposed for the causes of diabetes-induced malformations, such as disturbances in the metabolism of inositol, prostaglandins, and ROS (9). Beneficial effects on embryonic development in diabetes have been reported subsequent to dietary supplementation with inositol, arachidonic acid, and antioxidants both in vitro and in vivo (10 -14). A unifying etiology has been proposed, suggesting that excess glucose causes increased leakage of ROS from the mitochondrion. The ROS will affect second messenger systems, including prostaglandins synthesized from arachidonic acid (9). Most of the experiments supporting this hypothesis have been performed in rats with neural tube defects as the main outcome measure.Mechanistic data on bone mineralization defects in diabetes are less abundant than for embryonic dysmorphogenesis. Two fundamental mechanisms have been proposed to explain the ossification defects in offspring of diabetic rats, pinpointing either the Ca 2ϩ supply or the bone maturation itself as being disturbed by diabetes. The "push" model suggests that supply of Ca 2ϩ to the fetus is deficient, either through excessive Ca 2ϩ loss in maternal urine (15)

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Calcium metabolism in diabetic mother, fetus, and newborn infant

Cited by 34 publications

References 15 publications

Altered calbindin mRNA expression and calcium regulating hormones in rat diabetic pregnancy

Altered calbindin mRNA expression and calcium regulating hormones in rat diabetic pregnancy

Effect of <i>Cissus quadrangularis</i> Linn on skeletal growth in the neonates of diabetic rats

Gamma-Linoleic Acid and Ascorbate Improves Skeletal Ossification in Offspring of Diabetic Rats

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Calcium metabolism in diabetic mother, fetus, and newborn infant

Cited by 34 publications

References 15 publications

Altered calbindin mRNA expression and calcium regulating hormones in rat diabetic pregnancy

Altered calbindin mRNA expression and calcium regulating hormones in rat diabetic pregnancy

Effect of &lt;i&gt;Cissus quadrangularis&lt;/i&gt; Linn on skeletal growth in the neonates of diabetic rats

Gamma-Linoleic Acid and Ascorbate Improves Skeletal Ossification in Offspring of Diabetic Rats

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Effect of <i>Cissus quadrangularis</i> Linn on skeletal growth in the neonates of diabetic rats