Cardiac muscle contractions and insulin induced CD36-mediated LCFA uptake and GLUT4-mediated glucose uptake both use different signaling pathways. With insulin it activates phosphatidyl-inositol-3 (PI-3) and cellular contractions activates 5 prime adenosine monophosphate kinase (AMPK). Substrate uptake induced by insulin is additive to contraction-induced substrate uptake. They found that both CD36 and GLUT4 reside in similar intracellular storage compartments as found when they identified GLUT4 that was both in large and small depos. This then represents GLUT4 specific pre-endosomal storage compartments and recycling endosomal compartments. The small depos were then subdivided into transferrin receptor-positive depots recruited by contractions and transferrin receptor-negative depots recruited by insulin. They saw that co-localization of CD36 and GLUT4 was not observed and thus concluded that GLUT4 specific pre-endosomal storage as an intracellular depot of CD36 could be
Cardiac muscle contractions and insulin induced CD36-mediated LCFA uptake and GLUT4-mediated glucose uptake both use different signaling pathways. With insulin it activates phosphatidyl-inositol-3 (PI-3) and cellular contractions activates 5 prime adenosine monophosphate kinase (AMPK). Substrate uptake induced by insulin is additive to contraction-induced substrate uptake. They found that both CD36 and GLUT4 reside in similar intracellular storage compartments as found when they identified GLUT4 that was both in large and small depos. This then represents GLUT4 specific pre-endosomal storage compartments and recycling endosomal compartments. The small depos were then subdivided into transferrin receptor-positive depots recruited by contractions and transferrin receptor-negative depots recruited by insulin. They saw that co-localization of CD36 and GLUT4 was not observed and thus concluded that GLUT4 specific pre-endosomal storage as an intracellular depot of CD36 could be