GLUT mediated glucose transport across plasma membrane is gradient dependent and hexokinase activity may increase the rate of glucose uptake by altering the sugar in to an impermeant hexose phosphate. As hexokinase could be influenced by different signalling compounds governed by d opioid receptors, it was critical to assess if the d opioid stimulation was dependent on sugar metabolism. We found that GW0742 SNC 80 increased the uptake of 3 OMG, which can be not digested by hexokinase, to the same level as that of 2 deoxy N glucose, showing that the result was not dependent on increased hexokinase activity. Kinetic analysis indicated that d opioid receptor activation caused a rise in the maximal rate of glucose transport without affecting the clear affinity for the substrate. These changes may declare that d opioid receptor stimulated the uptake by enhancing the amount of transport molecules in the plasma membrane. It’s well-known that in skeletal muscle and adipose Metastatic carcinoma tissue, insulin stimulates glucose transport mainly by selling GLUT4 redistribution from cytoplasmic retailers to plasma membrane. In CHO cells overexpressing the human insulin receptor, insulin stimulation of glucose uptake was found to be associated with a growth in cell surface GLUT1 levels. We initially investigated the nature of GLUT molecular forms within CHO/ DOR cells, to examine the effects of n opioid receptor activation on mobile GLUT dynamics. Early functional studies reported the presence of only GLUT1 in CHO K1 cells, while a recent research employing primers for the human cDNA sequence and reverse transcription polymerase chain reaction also reported the presence of GLUT3 messenger RNA, though at a level lower than GLUT1 messenger RNA. In cells, we detected strong GLUT1, but no GLUT4 and GLUT3, Lenalidomide Revlimid immunoreactivity. These data are in line with previous studies reporting the absence of endogenous GLUT3 and GLUT4 proteins in CHO/K1 cells. Through the use of either floor protein biotinylation or subcellular membrane fractionation, we found that n opioid receptor activation of glucose uptake occurred in the absence of major changes in GLUT1 plasma membrane expression. A possible explanation with this finding is that the methods used failed to detect subtle but functionally significant changes in glucose transporter trafficking to the cell surface. Using the same methods, nevertheless, other studies found alterations in cellular GLUT1 distribution following hormonal stimulation. This kind of legislation has been suggested for other stimuli, including inhibition of osmotic stress and oxidative phosphorylation, that have also been found to improve glucose transportation without affecting membrane GLUT1 levels.