Several studies have reported that almost all protease inhibitors (PIs) can cause IR, effects likely caused by the inhibition of glucose transport mediated by glucose transporter type 4 (GLUT-4) [ 5, 6].
However, currently, the mechanisms related to glycogen and glucose transport are uncertain; although, some authors believe that glycogen could regulate glucose transport by agglutination of glucose transporter type 4 (GLUT4) molecules and further incorporation into glycogen complex and enzymes.
Muscle-specific glucose transporter type 4 (GLUT4) plays an important role in the transport of glucose inside the cells when the mechanism is insulin-independent [4, 6].
Insulin and muscle contractions stimulate glucose transport in skeletal muscle via translocation of intracellular glucose transporter type 4 (GLUto) thethe cell surface.
(b) Glycine transporter type 1 (GlyT1) inhibitor, which has shown potential in the treatment of schizophrenia, containing a F-substituted benzyl-amine moiety.
Martina, M. et al. Glycine transporter type 1 blockade changes NMDA receptor-mediated responses and LTP in hippocampal CA1 pyramidal cells by altering extracellular glycine levels.
Vesicular monoamine transporter type 2 (VMAT2) is a newly emerging target for both diagnostic and therapeutic applications in diabetes mellitus.
Writing in the online edition of Physiological Genomics, researchers from the University of Toronto say the gene, glucose transporter type 2, helps the brain regulate the intake of food.
Various culture matrices influenced the expression of glucose transporter type 2 and gluco kinase, being they expressed more intensively on PLL rather than C or in controls.
Insulin signaling seems intact, and the abundance and localization of the major fatty acid and glucose transporters, CD36 (cluster of differentiation 36) and GLUT4 (glucose transporter type 4), are also unchanged.
Martina M, B-Turcotte ME, Halman S, Tsai G, Tiberi M, Coyle JT, Bergeron R. Reduced glycine transporter type 1 expression leads to major changes in glutamatergic neurotransmission of CA1 hippocampal neurones in mice.
