Muscle glucose transporter

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). 

Hansen, R, Gulve, E., Marshall, B., Gao, J. Pessin, J., HoUoszy, J., and Mueckler, M. (1995). Skeletal muscle glucose transport and metabolism are enhanced in transgenic mice overexpressing the glut4 glucose transporter. J. Biol. Chem. 270,1679-1684. 

Insulin increases muscle glucose transporters and androgen receptors... 

Diets containing n-3 PUFA have also been observed to decrease body weight of diabetic (streptozotocin-treated) rats. Such diets increased responsiveness of muscle glucose transport to insulin (22), and raised plasma leptin levels which, in turn, is associated with decreased food intake (23). 

Henriksen, E.J., M.K. Teachey, Z.C. Taylor, S. Jacob, A. Ftock, K. Kramer, and O. Hsselwander. Isomer-Specific Actions of Conjugated Linoleic Acid on Muscle Glucose Transport in the Obese Zucker Rat,.d ./. Physiol 285 E98—E105 (2003). 

Henriksen, E.J., Teachey, M.K., Taylor, Z.C., Jacob, S., Saengsirisuwan, V., Kramer, K., Klatt, M.J., Ptock, A., and Hasselwander, O. (2002) Metabolic Effects of Conjugated Linoleic Acid on Insulin Resistant Rat Skeletal Muscle Glucose Transport Are Isomer Specific, Diabetes 51, A309 (Abstr.). 

The absorption of sulfonylureas from the upper gastrointestinal tract is faidy rapid and complete. The agents are transported in the blood as protein-bound complexes. As they are released from protein-binding sites, the free (unbound) form becomes available for diffusion into tissues and to sites of action. Specific receptors are present on pancreatic islet P-ceU surfaces which bind sulfonylureas with high affinity. Binding of sulfonylureas to these receptors appears to be coupled to an ATP-sensitive channel to stimulate insulin secretion. These agents may also potentiate insulin-stimulated glucose transport in adipose tissue and skeletal muscle. 

In addition to secretory cells, many non-secretory cells are capable of regulating exocytotic fusion of transport vesicles that are derived from endosomal precursors. For instance, vesicles enriched in plasma membrane transport proteins are incorporated in a regulated manner in order to alter metabolite fluxes. Examples include the glucose transporter GLUT-4 in muscle and fat tissues, a key element in the control of... 

At present, the only available drug that stimulates glucose transport is insulin. Insulin increases the abundance of the GLUT4 in plasma membranes of adipose and muscle cells by its recruitment from intracellular storage sites (for a detailed description of its mechanism, see Chapter Diabetes Mellitus). 

GLUT4 is a glucose transporter exclusively expressed in tissues with insulin-sensitive glucose uptake (heart, muscle, fat). Under basal conditions, GLUT4 is predominantly located in intracellular vesicles, and is... 

Skeletal muscle Increased glucose transport GLUT4-translocation see above (fat)... 

The entry rate of glucose into red blood cells is far greater than would be calculated for simple diffusion. Rather, it is an example of facilitated diffiision (Chapter 41). The specific protein involved in this process is called the glucose transporter or glucose permease. Some of its properties are summarized in Table 52-3-The process of entry of glucose into red blood cells is of major importance because it is the major fuel supply for these cells. About seven different but related glucose transporters have been isolated from various tissues unlike the red cell transporter, some of these are insidin-dependent (eg, in muscle and adipose tissue). There is considerable interest in the latter types of transporter because defects in their recruitment from intracellular sites to the surface of skeletal muscle cells may help explain the insulin resistance displayed by patients with type 2 diabetes mellitus. 

Fukumoto, H., et al. Cloning and characterization of the major insulin-responsive glucose transporter expressed in human skeletal muscle and other insulin-responsive tissues. J. Biol. Chem. 1989, 264, 7776-7779. 

Doege, H., et al. Characterization of human glucose transporter (GLUT) 11 (encoded by SLC2A11), a novel sugar-transport facilitator specifically expressed in heart and skeletal muscle. Biochem. J. 2001, 359, 443-449. 

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