Effect of chromium citrate on the mechanism of glucose transport and insulin resistance in Buffalo rat liver cells.

OBJECTIVE: Our published literature indicated that chromium citrate could regulate the glycemic index in alloxaninduced diabetic mice. The present study investigated the mechanism of chromium citrate in insulin resistance (IR) buffalo rat liver (BRL) cells. MATERIALS And METHODS: Chromium citrate was synthesized in our laboratory. BRL cells were purchased from the Chinese Academy of Sciences Cell Bank. The glucose transport and IR affected by chromium citrate in BRL cells were examined. The Thiazolyl Blue Tetrazolium Bromide (MTT) and glucose assay experiments were measured by microplate ELISA reader. The protein kinase B (Akt), glucose transporter-4 (Glut4), and phosphor-AMP-activated protein kinase beta1 levels were tested by Western blot, and the mRNA expression of glucose transport proteins (Akt2, Glut4, and AMPactivated protein kinase alpha2 (AMPKalpha2)) and insulin sensitivity proteins (insulin receptor substrate1 (IRS-1), phosphatidylinositol 3 kinase (PI3K), and peroxisome proliferator-activated receptor gamma (PPARgamma)) was measured by reverse transcription-polymerase chain reaction. RESULTS: The results indicated that the glucose absorption level of chromium citrate groups was higher than model group significantly. It demonstrated that chromium citrate could significantly improve glucose absorption in IR BRL cells. The Akt, Glut4, and phosphor-AMPKbeta1 levels in chromium citrate groups (at doses of 0.4, 0.2, and 0.1 mug Cr/mL) were markedly improved when compared with the other experiment groups, and chromium citrate could more effectively increase the Akt level than chromium trichloride. In addition, the mRNA expression of Akt2, Glut4, and AMPKalpha2 in chromium citrate groups was significantly improved when contrasted with model group. CONCLUSION: The consequences illustrated that chromium citrate can affect the IR BRL cells' ameliorating glucose transport and IR.