Objective: To study the regulation of chromium on the related gene expression of glucose metabolism in skeletal muscle in diabetic rats. Methods: cDNA fragments were cloned, sequenced from our former research and its homology analysis has been done. RT-PCR was performed using the primers designd according to the sequence of cDNA. Results: The sequence identities between Cr-3 and GLUT4 were 98%. The GLUT4 mRNA expression level of DM+Cr group was obviously lower than that of normal group (P

Objective: To study the effects of chromium on glucose and lipid metabolism and gene expression in diabetic rats.Methods: Male Wistar rats were assigned to three groups:normal control(NC), alloxan-induced diabetic control group(DM), and DM with chromium supplementation group(DM+Cr). Cr 200 ?g/(kg bw?d) was supplemented orally for 60 days. At the end of the treatment, the blood glucose, lipid and serum insulin were measured, and the changes in gene expression among three groups were studied by mRNA differential display technique.Results: Blood glucose in DM+Cr group decreased significantly than that before experiment. The levels of serum TG, TC, LDL-C and AI in DM+Cr group were lower than those of DM group, while the serum HDL-C levels were higher. Serum insulin was not improved obviously in DM+Cr group. 11 cDNA fragments larger than 400 bp expressed differences in skeletal muscles between DM+Cr group and DM group and were isolated, 4 of which expressed higher in DM+Cr group, while the rest expressed higher in DM group.Conclusion: Chromium supplementation could partially improve the disorders of glucose and lipid metabolism, and have an impact on some gene expression in diabetic rats, which may contribute to the regulating effects on its disorders of metabolism.

BACKGROUND:Cerebral white matter demyelination is outstanding in the images of delayed encephalopathy after acute carbon monoxide (CO) poisoning. Since Nogo-A and Nogo-receptor are expressed in onoligodendrocytes and neurons respectively, we infer that Nogo-A system is involved in brain injury after acute CO poisoning and related to delayed encephalopathy after acute CO poisoning. Endogenous CO is a gaseous messenger, which is the metabolic product of hemeoxygenase. There is no report about the CO effect on Nogo-A system til now. OBIECTIVE: To in vitro culture oligodendrocytes using endogenous CO, inhibit the activity of hemeoxygenase system using zinc protoporphyrin-IX (ZnPPIX) and observe the variation of Nogo-A in oligodendrocytes at mRNA and protein levels. METHODS: Rat oligodendrocytes cultured in vitro were divided into control, CO, ZnPPIX groups. Cels in the CO and ZnPPIX groups were treated with 1% CO directly, In the ZnPPIX group, 10 μmol/L ZnPPIX was added into the culture medium before CO treatment. The expressions of Nogo-A mRNA and protein at 6, 24, 48 hours after culture were compared. Differences in the peak levels of Nogo-A mRNA and protein between CO and ZnPPIX groups were detected using RT-PCR and immunohistochemistry respectively. RESULTS: The expression levels of Nogo-A mRNA and protein were significantly higher in the CO group than the control group and reached the peak at 24 hours of culture. Compared with the CO group, oligodendrocytes cultured with ZnPPIX showed higher expressions of Nogo-A mRNA and protein at 24 hours of culture. These findings suggest that except the influence of hypoxia occurring in CO poisoning, exogenous CO increases the expression of Nogo-A in cultured oligodendrocytes in vitro, and the heme oxygenase system can inhibit the expression of Nogo-A mRNA and protein.