Maternal hypomagnesemia causes placental abnormalities and fetal and postnatal mortality.
BACKGROUND
Magnesium (Mg(2+)) is essential for cellular growth and the maintenance of normal cellular processes. However, little is known about how maternal hypomagnesemia during pregnancy affects fetal growth and development. This study investigated the effects of maternal hypomagnesemia on the late gestation placenta and fetus, and postnatal outcomes until weaning.


METHODS
Female CD1 mice consumed a control (0.2% w/w Mg(2+)), moderately Mg(2+) deficient (MMD; 0.02% w/w Mg(2+)) or severely Mg(2+) deficient (SMD; 0.005% w/w Mg(2+)) diet for 4 weeks prior to mating and throughout pregnancy. Dams were killed at E18.5 for embryonic studies or allowed to litter naturally and the offspring studied up to postnatal day 21.


RESULTS
At E18.5, both Mg(2+) deficient diets decreased maternal plasma and bone Mg(2+) but only the SMD diet decreased fetal plasma Mg(2+). Maternal hypomagnesemia led to fetal loss and fetal growth restriction. Maternal Mg(2+) deficiency increased placental glycogen cell area and decreased spongiotrophoblast cell area while upregulating mRNA expression of the MagT1 Mg(2+) transporter in spongiotrophoblast cells. The SMD animals also displayed instances of gross placental abnormalities. After birth, pups in the SMD group had increased early postnatal mortality and failed to thrive. Pups in the MMD group underwent catch-up growth but remained shorter than controls at PN21 and were hypomagnesemic and hypoglycemic.


CONCLUSIONS
These changes suggest that maternal Mg(2+) deficiency during pregnancy impairs placental development and fetal growth, which may have long-term health consequences for offspring. Collectively, these results have important implications for women who are Mg(2+) deficient during pregnancy.
School of Biomedical Sciences, The University of Queensland, Brisbane, Australia.
R N
RN
Schlegel
School of Biomedical Sciences, The University of Queensland, Brisbane, Australia.
J S M
JS
Cuffe
School of Biomedical Sciences, The University of Queensland, Brisbane, Australia.
K M
KM
Moritz
School of Biomedical Sciences, The University of Queensland, Brisbane, Australia. Electronic address: t.paravicini@uq.edu.au.
T M
TM
Paravicini
D000818:Animals; D001842:Bone and Bones / Q000737:chemistry; D027682:Cation Transport Proteins / Q000235:genetics; D004032:Diet; D005260:Female; D005313:Fetal Death / Q000209:etiology*; D047109:Fetal Development; D005317:Fetal Growth Retardation / Q000209:etiology; D005865:Gestational Age; D008274:Magnesium / Q000008:administration & dosage / Q000032:analysis / Q000097:blood; D008275:Magnesium Deficiency / Q000150:complications*; D051379:Mice; D010920:Placenta / Q000473:pathology / Q000503:physiopathology; D010922:Placenta Diseases / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D010929:Placentation; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology*; D011297:Prenatal Exposure Delayed Effects / Q000401:mortality / Q000473:pathology; D012333:RNA, Messenger / Q000032:analysis; D014327:Trophoblasts / Q000737:chemistry / Q000473:pathology
D027682:Cation Transport Proteins; D012333:RNA, Messenger; D008274:Magnesium
Fetal growth restriction; Hypomagnesemia; Mg(2+) channels; Placental glycogen