Figure 8.

Proposed model describing the effects of maternal Mg deficiency in mice during pregnancy. On the maternal side, Mg deficiency is accompanied by higher maternal circulating glucose and insulin, positive regulators of Srebf1 and Chrebp mRNA expression, which promote Fasn and Acaca mRNA expression. Together, these promote higher hepatic SFAs, along with Scd1, D5d, D6d (desaturase) and Elovl1, Elovl2, Elovl5 and Elovl6 (elongase) mRNA expression, which lead to higher circulating FFAs and hepatic SFAs and MUFAs and lower hepatic PUFAs, specifically DHA and AA (which are negative regulators of Srebf1 and Chrebp mRNA expression). On the fetal side, Mg deficiency is accompanied by no changes in glucose or insulin concentrations, consistent with no changes in Srebf1 and Chrebp mRNA expression in the fetal liver. Inadequate supplies of maternal DHA and AA, which are critical for fetal growth and brain development, lead to lower fetal brain DHA concentrations along with a compensatory increase in fetal hepatic PUFAs (DHA and AA) and decrease in MUFAs (via decreased Fasn, Acaca, Scd1 and Elovl6 mRNA expression). Maternal and fetal metabolic dysfunction during Mg deficiency is accompanied by fetal growth restriction and increased fetal mortality.