Magnesium supplementation affects gene expression related to insulin and lipid in patients with gestational diabetes

Mehri Jamilian1, Mansooreh Samimi2, Afshar Ebrahimi Faraneh2

  • 1Endocrinology and Metabolism Research Center, Department of Gynecology and Obstetrics, School of Medicine, Arak University of Medical Sciences, Arak, Iran.

Magnesium Research
|December 20, 2017
PubMed

Magnesium is known to exert several beneficial effects, including antiglycemic and antilipidemic properties. The aim of this study was to evaluate the effects of magnesium supplementation on gene expression related to insulin and lipid metabolism in women with gestational diabetes (GDM) who were not on oral hypoglycemic agents. This randomized double-blind, placebo-controlled trial was conducted among 40 patients diagnosed with GDM, aged 18-40 years. Participants were randomly allocated into two groups to take either 250 mg/day of magnesium supplements in the form of magnesium oxide (n = 20) or placebo (n = 20) for 6 weeks. Gene expression related to insulin and lipid metabolism was assessed in peripheral blood mononuclear cells (PBMCs) of women with GDM using RT-PCR method. Compared with the placebo, magnesium supplementation to women with GDM resulted in a significant decrease in levels of fasting plasma glucose (FPG) (-9.7 ± 5.6 vs. -0.1 ± 8.5 mg/dL, P<0.001). Quantitative results of RT-PCR demonstrated that compared with the placebo, magnesium supplementation upregulated gene expression of peroxisome proliferator-activated receptor gamma (PPAR-γ) (P = 0.003) and glucose transporter 1 (GLUT-1) (P = 0.004) and downregulated gene expression of oxidized low-density lipoprotein receptor (LDLR) (P = 0.001) in PBMCs of women with GDM. In addition, a trend toward a greater decrease in gene expression of lipoprotein (a) [LP(a)] was observed in the patients belonging to magnesium group compared to placebo group (P = 0.08). Overall, magnesium supplementation for 6 weeks in women with GDM significantly improved FPG levels, and gene expression of PPAR-γ, GLUT-1, and LDLR.

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