The role of oral magnesium sulfate in the stimulation of PPAR-γ and inhibition of NFKB genes expression in improving hyperglycemia in the muscle of STZ-induced diabetic rat

Introduction: The aim of this study was to investigate the possible role of magnesium (Mg2+) on activation of the peroxisome proliferator-activated receptor gamma (PPAR-γ) and inhibition of nuclear factor-KB (NFKB p65) in muscle to increase glucose transporter 4 (GLUT4) gene expression.Methods. Fifty rats were divided into five groups, namely non-diabetic control (NDC), Mg2+-treated non-diabetic control (Mg2+-NDC), chronic diabetic (CD), Mg2+-treated chronic diabetic (Mg2+-CD), and insulin-treated chronic diabetic (Ins-CD). Diabetes was induced with streptozotocin (STZ) injection. The Mg2+-CD and Mg2+-NDC groups received 10g/l of magnesium sulfate (MgSO4) added to drinking water and Ins-CD group received 2.5 U/kg of insulin. The fasting blood glucose level and body weight were measured every week. After 16 weeks, intraperitoneal glucose tolerance test (IPGTT) was done and then animals were decapitated, blood samples were taken to determine the plasma levels of Mg2+ and gastrocnemius muscle legs were isolated for both PPAR-γ and NFKB (p65) genes and proteins expression.Results. Administration of MgSO4 improved IPGTT, lowered blood glucose levels and increased PPAR-γ gene and protein expression. Diabetes increased NFKB gene and protein expression. Although Mg2+ therapy could not decrease NFKB (p65) gene expression, the protein decreased by Mg2+ therapy. Insulin decreased NFKB (p65) gene and protein expression, without any effect on PPAR-γ gene and protein expression.Conclusion. Findings suggested that Mg2+ decreases blood glucose levels via suppressing NFKB (p65) protein synthesis and increases PPAR-γ gene and protein expression. But insulin could decrease blood glucose level through a decrease in NFKB (p65) gene and protein expression.

کلیدواژه ها:

Diabetes ، Insulin ، Magnesium ، PPAR-γ ، NFKB (p65)