Hypocalcemia in infants of diabetic mothers

Tsang, Reginald C.; Kleinman, Leonard I.; Sutherland, James M.; Light, Irwin J.

doi:10.1016/s0022-3476(72)80494-3

Cited by 132 publications

(30 citation statements)

References 21 publications

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“…Significant alterations in calcium homeostasis occur in up to 50% of infants born to insulin-dependent diabetic mothers (Tsang et al 1972). Such children have an increased incidence of hypocalcaemia (Tsang et al 1972, Mimouni et al 1986 and either a decreased (Lapillone et al 1997) or an increased (Mimouni et al 1988) bone mineral content compared with normal infants.…”

Section: Introductionmentioning

confidence: 99%

“…Such children have an increased incidence of hypocalcaemia (Tsang et al 1972, Mimouni et al 1986 and either a decreased (Lapillone et al 1997) or an increased (Mimouni et al 1988) bone mineral content compared with normal infants. A reduced bone mineral content, retarded skeletal development, or both, is found in the offspring of genetically diabetic rats (Verhaeghe et al 1988a) and those rendered diabetic by streptozotocin (STZ; Uriu-Hare et al 1985, Demignon & Bonneton-Rebut 1988.…”

Section: Introductionmentioning

confidence: 99%

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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: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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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“…Low values of PTH in comparison with adult standards were found in both groups of infants, despite de creasing calcium levels. A hypothesis is presented to account for early neonatal hypo calcemia (NHC) in IDM.Neonatal hypocalcemia (NHC) during the first days of life occurs more often in infants of diabetic mothers (IDM) than in normal infants, even when gestational age and perinatal complications are taken into consideration [13].Several mechanisms have been suggested as the possible cause of NHC. Among these are: fetal hypoparathyroidism because of relative hyper parathyroidism in the mother [13], end-organ unresponsiveness to the parathyroid hormone (PTH) [7], and hyperphosphatemia caused by tissue breakdown [13,15],…”

mentioning

confidence: 99%

Calcitonin and Parathyroid Hormone – Relation to Early Neonatal Hypocalcemia in Infants of Diabetic Mothers

Bergman

Kjellmer

Selstam³

1974

Neonatology

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The levels of total and ultrafiltrable calcium, phosphorus, total protein, calcitonin (CT) and parathyroid hormone (PTH) in plasma were determined together with blood sugar in 11 consecutive cases of infants of diabetic mothers (IDM) and 9 healthy term infants during the first days of life. The decrease of calcium in plasma after birth was significantly greater in IDM than in controls. In both IDM and controls, a marked increase of the CT concentration was observed after birth. The maximum was reached at 24 h of age. No significant differences were seen between the two groups. Only in IDM was a significant correlation between calcium and CT in plasma seen, suggesting a greater sensitivity to CT in these infants. Low values of PTH in comparison with adult standards were found in both groups of infants, despite decreasing calcium levels. A hypothesis is presented to account for early neonatal hypocalcemia (NHC) in IDM.

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“…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)(2)(3)(4). In addition, hypocalcemia and reduced bone mineral content are found in neonates of diabetic mothers (3,(5)(6)(7).…”

mentioning

confidence: 99%

“…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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Hypocalcemia in infants of diabetic mothers

Cited by 132 publications

References 21 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

Calcitonin and Parathyroid Hormone – Relation to Early Neonatal Hypocalcemia in Infants of Diabetic Mothers

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

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