The role of PPAR-γ and NFKB genes expression in muscle to improve hyperglycemia in STZ-induced diabetic rat following magnesium sulfate administration.

The present study was designed 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. 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 10 g/l of magnesium sulfate (MgSO4 ) added to drinking water and Ins-CD group received 2.5 U/kg of insulin. The 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. 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. According to our findings it seems that suppressing NFKB (p65) protein synthesis and increases in PPAR-γ gene and protein expression could help Mg2+ administration to decreases blood glucose levels. But decreasing in NFKB (p65) gene and protein expression help insulin to decrease blood glucose level.