A role for magnesium in neonatal parathyroid gland function?

Loughead, Jeffrey L.; Mimouni, Francis; Tsang, Reginald C.

doi:10.1080/07315724.1991.10718135

Cited by 23 publications

(10 citation statements)

References 29 publications

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“…This inhibits bone resorption and results in hypocalcemia despite low PTH concentrations. Loughead et al (47) suggested that hypomagnesemia blunts the parathyroid secretory response to hypocalcemia, leading to an inappropriately low PTH concentration. However, these proposed mechanisms do not account for the observations made in the current study.…”

Section: Discussionmentioning

confidence: 99%

Increased Renal Tubular Reabsorption of Calcium and Magnesium by the Offspring of Diabetic Rat Pregnancy

et al. 2005

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Diabetic pregnancy has a marked influence on offspring calcium and magnesium homeostasis. Urinary excretion of calcium and magnesium is reduced, yet offspring of diabetic pregnancy exhibit hypomagnesemia and hypocalcemia. The aim of this study was to measure renal hemodynamic and tubular function in the offspring of diabetic (OD) and control, nondiabetic (OC) rats at 4 and 8 wk of age to determine the glomerular and tubular mechanisms through which renal calcium and magnesium handling are programmed in utero. The fraction of filtered calcium that was excreted was significantly lower in OD at both 4 and 8 wk of age [8 wk: OC (n ϭ 6), 11.8 Ϯ 2.9 versus OD (n ϭ 5), 4.3 Ϯ 0.6%; p Ͻ 0.05] and that of magnesium was lower at 8 wk of age [OC (n ϭ 6), 42.4 Ϯ 7.5 versus OD (n ϭ 5), 13.0 Ϯ 1.7%; p Ͻ 0.01]. This increased reabsorption occurred despite an elevated GFR in OD. These findings clearly indicate that tubular reabsorptive mechanisms for calcium and magnesium are increased markedly in OD. Serum PTH concentration was reduced in 8-wk-old OD [OC (n ϭ 7), 539.4 Ϯ 142.1 versus OD (n ϭ 9), 174.3 Ϯ 69.4 pg/ml; p Ͻ 0.05], consistent with previous reports in human infants. Taken together, these observations suggest that the basis for the altered renal magnesium and calcium handling in OD involves increased tubular transport activity and possibly increased sensitivity of these mechanisms to PTH. Diabetic pregnancy has a marked impact on maternal calcium and magnesium homeostasis in both humans and rats. Hypomagnesemia has been widely reported in human diabetic pregnancy (1-3), and diabetic pregnant rats display a marked increase in urinary magnesium excretion (4,5). A reduction in third-trimester plasma calcium concentration has been observed in human diabetic pregnancy in one study (3), but the majority of studies have found no difference in calcium concentrations between normal and diabetic pregnancies. However, in the diabetic rat, pregnancy is associated with marked increases in urinary calcium (4,5) and hypocalcemia in some (4) but not all studies (6).These changes in maternal divalent ion handling have a profound impact on the developing fetus. Human offspring of diabetic pregnancy exhibit hypomagnesemia and hypocalcemia as neonates (2,7-9). In the rat, renal handling of calcium and magnesium is also altered in the offspring of streptozotocin (STZ)-treated diabetic rats (OD). We recently reported that OD retain both calcium and magnesium as neonates and that this continues into adulthood (10). These changes in divalent ion homeostasis also occur in conjunction with changes in bone structure. Human offspring of diabetic pregnancy are susceptible to congenital malformations, including skeletal abnormalities (11), and have lower bone mineral content (12). Reduced bone mineral content and abnormal skeletal development have also been observed in the offspring of STZ-treated diabetic rat mothers (13,14). We recently extended these observations and showed that offspring of STZ-treated diabetic rats have reduced trabecular and ...

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Section: Discussionmentioning

confidence: 99%

Increased Renal Tubular Reabsorption of Calcium and Magnesium by the Offspring of Diabetic Rat Pregnancy

et al. 2005

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“…Subsequent studies used intact PTH assays but obtained measurements solely at birth and 24 h later, and demonstrated that PTH rose significantly (31,386,388,416,444,473,580). Those studies did not determine when the PTH value increased or whether the peak level was achieved at 24 h or later.…”

Section: Human Datamentioning

confidence: 99%

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Kovacs

2014

Physiological Reviews

211

188

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Mineral and bone metabolism are regulated differently in utero compared with the adult. The fetal kidneys, intestines, and skeleton are not dominant sources of mineral supply for the fetus. Instead, the placenta meets the fetal need for mineral by actively transporting calcium, phosphorus, and magnesium from the maternal circulation. These minerals are maintained in the fetal circulation at higher concentrations than in the mother and normal adult, and such high levels appear necessary for the developing skeleton to accrete a normal amount of mineral by term. Parathyroid hormone (PTH) and calcitriol circulate at low concentrations in the fetal circulation. Fetal bone development and the regulation of serum minerals are critically dependent on PTH and PTH-related protein, but not vitamin D/calcitriol, fibroblast growth factor-23, calcitonin, or the sex steroids. After birth, the serum calcium falls and phosphorus rises before gradually reaching adult values over the subsequent 24 -48 h. The intestines are the main source of mineral for the neonate, while the kidneys reabsorb mineral, and bone turnover contributes mineral to the circulation. This switch in the regulation of mineral homeostasis is triggered by loss of the placenta and a postnatal fall in serum calcium, and is followed in sequence by a rise in PTH and then an increase in calcitriol. Intestinal calcium absorption is initially a passive process facilitated by lactose, but later becomes active and calcitriol-dependent. However, calcitriol's role can be bypassed by increasing the calcium content of the diet, or by parenteral administration of calcium.

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“…Normal cord blood values for our laboratory vary between 9.0 and 11.4 mg/dl for calcium 15 and 1.74 and 1.90 mg/dl for magnesium. 16 Serum ionized calcium was measured using a Radiometer ICA 1, ion-selective electrode (Radiometer, Coppenhagen). 17 The normal range in nonpregnant adults in our laboratory is 4.8 to 5.2 and is 4.4 to 5.4 mg/dl for neonates (CV, 1.4%).…”

Section: Methodsmentioning

confidence: 99%

Spectrum and Natural History of Congenital Hyperparathyroidism Secondary to Maternal Hypocalcemia

Loughead

Mughal²,

Mimouni³

et al. 1990

Amer J Perinatol

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Fourteen cases of congenital hyperparathyroidism secondary to maternal hypocalcemia have been reported. We report two additional cases that highlight the wide spectrum of the disease. We extensively studied the parathyroid function of these infants to test the hypothesis that the biochemical hyperparathyroidism found in these infants would be transient in nature, since the presumed etiology (maternal and subsequent fetal hypocalcemia) should disappear soon after birth with establishment of enteral feedings. Infant 1 was born to a mother with idiopathic hypoparathyroidism with poor compliance to therapy and documented hypocalcemia in pregnancy. Severe congenital demineralization and intrauterine fractures with clinical and radiologic bowing of the long bones were obvious. Bone mineral content and bone mineral content/bone width ratio, measured by photon absorptiometry, were both markedly below normal. Infant 2 was born to a mother with postsurgical hypoparathyroidism with excellent compliance. The mother was normocalcemic. The infant was clinically and radiologically asymptomatic. The bone mineral content was just at the lower limit of normal, but bone mineral content/bone width ratio was below the normal limits. Biochemical features include elevation of cord serum parathyroid hormone (1-84, radioimmunoassay) in both cases, coexisting with serum calcium, phosphorus concentrations within normal limits. Serum parathyroid hormone fell to within normal ranges by 9 days of age in both infants. With no treatment, bone mineral content at 1 month of age was normal in both infants.

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A role for magnesium in neonatal parathyroid gland function?

Cited by 23 publications

References 29 publications

Increased Renal Tubular Reabsorption of Calcium and Magnesium by the Offspring of Diabetic Rat Pregnancy

Increased Renal Tubular Reabsorption of Calcium and Magnesium by the Offspring of Diabetic Rat Pregnancy

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Spectrum and Natural History of Congenital Hyperparathyroidism Secondary to Maternal Hypocalcemia

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