Glucose transporter effects

Simpson, I. A., Appel, N. M., Hokari, M. etal. Blood-brain barrier glucose transporter effects of hypo- and hyperglycemia revisited. /. Neurochem. 72 238-247,1999. 

Blood-brain barrier glucose transporter Effects of hypo-and hyperglycemia revisited. J Neurochem 72 238-247. 

The insulin receptor is a transmembrane receptor tyrosine kinase located in the plasma membrane of insulin-sensitive cells (e.g., adipocytes, myocytes, hepatocytes). It mediates the effect of insulin on specific cellular responses (e.g., glucose transport, glycogen synthesis, lipid synthesis, protein synthesis). 

Transport asymmetry and the effect of cytoplasmic ATP The results of many kinetic studies have shown that glucose transport in the erythrocyte is markedly asymmetric, the and F ax values for zero-tram efflux being substantially greater than the corresponding values for influx, particularly at low... 

The effects of D-glucose observed in vivo are not well reproduced in vitro. Madara [203] reported that cytoskeletal contraction and enhanced paracellular permeability were observed only in an in situ perfusion preparation and not in an isolated tissue preparation. Although its in vivo effect was not tested, 25 mM D-glucose, an effective concentration in the jejunum [47], failed to enhance the in vitro transport of sotalol (log PC = -0.62), atenolol (log PC = 0.16), or nadolol (log PC = 0.93) across the isolated conjunctiva [213], For a similar reason and possibly due to the absence of a Na+-glucose cotransporter in the cornea, 25 mM D-glucose was ineffective in increasing the corneal transport of these three drugs. 

Fihn, B. M., A. Sjoqvist, and M. Jodal. Permeability of the rat small intestinal epithelium along the villus-crypt axis effects of glucose transport, Gastroenterology 2000, 119, 1029-1036... 

J.A. Tamada and K. Comyns, Effect of formulation factors on electroosmotic glucose transport through human skin in vivo. J. Pharmaceutical Sci. 94, 1839-1849 (2005). 

To Study the Effect Of Urtica Dioica Extract On Diabetes-Mediated Alteration in Glucose Transporter. 

Figure 5.9 The sodium ion/glucose transporter and sodium ion/ amino acid transporter. The biochemistry of the two processes is identical. To maintain electroneutral transport K ion replaces Na ion, via NaVK ATPase. The broader arrow indicates overall effect (i.e. unidirectional) transport.

In skeletal muscle, glucose transport is non-equilibrium, so that an increase in activity of the transporter increases glucose utilisation. Factors that increase the activity of the transporter (e.g. the number of transporter molecules) in the membrane are insulin and sustained physical activity. In contrast, the hormone cortisol decreases the number of transporters in the membrane. This decreases glucose uptake and is one of the effects of cortisol that helps to maintain the normal blood glucose level (Chapter 12). 

Figure 6.15 Regulation of the number of glucose transporters in the plasma membrane. The transporter affected is GLUT-4. It is unclear which translocation process is affected by insulin, physical activity or a change in the ATP/ADP concentration ratio. Effects on the translocation from within the cell to the membrane or vice versa are indicated here.

Figure 6.19 Regulation of the synthesis of glycogen from glucose in liver and muscle. Insulin is the major factor stimulating glycogen synthesis in muscle it increases glucose transport into the muscle and the activity of glycogen synthase, activity which is also activated by glucose 6-phosphate but inhibited by glycogen. The latter represents a feedback mechanism and the former a feedforward. The mechanism by which glycogen inhibits the activity is not known. The mechanism for the insulin effect is discussed in Chapter 12.

Activation of a protein kinase that is responsible for many of the metabolic effects, for example increased activity of glycogen synthase, increased translocation of the glucose transporter molecules to the plasma membrane and increased activity of acetyl-CoA carboxylase. 

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