Each of the four intracellular cysteines of CD36 is essential for insulin- or AMP-activated protein kinase-induced CD36 translocation.

Stimulation of cellular fatty acid uptake by induction of insulin signalling or AMP-kinase (AMPK) activation is due to translocation of the fatty acid-transporter CD36 from intracellular stores to the plasma membrane (PM). For investigating the role of the four Cys-residues within CD36's cytoplasmic tails in CD36 translocation, we constructed CHO-cells expressing CD36 mutants in which all four, two, or one of the intracellular Cys were replaced by Ser. Intracellular and PM localization of all mutants was similar to wild-type CD36 (CD36wt).

Insulin and chromium picolinate induce translocation of CD36 to the plasma membrane through different signaling pathways in 3T3-L1 adipocytes, and with a differential functionality of the CD36.

Chromium picolinate (CrPic) has been indicated to activate glucose transporter 4 (GLUT4) trafficking to the plasma membrane (PM) to enhance glucose uptake in 3T3-L1 adipocytes. In skeletal and heart muscle cells, insulin directs the intracellular trafficking of the fatty acid translocase/CD36 to induce the uptake of cellular long-chain fatty acid (LCFA). The current study describes the effects of CrPic and insulin on the translocation of CD36 from intracellular storage pools to the PM in 3T3-L1 adipocytes in comparison with that of GLUT4.

Effects of AMPK activators on the sub-cellular distribution of fatty acid transporters CD36 and FABPpm.

In heart and skeletal muscle, enhanced contractile activity induces an increase in the uptake of glucose and long-chain fatty acids (LCFA) via an AMP-activated protein kinase (AMPK)-regulated mechanism. AMPK activation induces glucose uptake through translocation of glucose transporter 4 (GLUT4) from intracellular pools to the plasma membrane (PM). AMPK-mediated LCFA uptake has been suggested to be regulated by a similar translocation of the LCFA transporters CD36 and plasma membrane-associated fatty acid binding protein (FABPpm).

Insulin-induced translocation of CD36 to the plasma membrane is reversible and shows similarity to that of GLUT4.

In cardiac and skeletal muscles, insulin regulates the uptake of long-chain fatty acid (LCFA) via the putative LCFA transporter CD36. Biochemical studies propose an insulin-induced translocation of CD36 from intracellular pools to the plasma membrane (PM), similar to glucose transporter 4 (GLUT4) translocation. To characterize insulin-induced CD36 translocation in intact cells, Chinese hamster ovary (CHO) cells stably expressing CD36 or myc-tagged GLUT4 (GLUT4myc) were created.

Fic1 is expressed at apical membranes of different epithelial cells in the digestive tract and is induced in the small intestine during postnatal development of mice.

Mutations in ATP8B1 are associated with FIC1 disease, an autosomal recessive disorder in which intrahepatic cholestasis is the predominant manifestation. ATP8B1 encodes FIC1, which is expressed in several tissues, most prominently in the intestine, pancreas, and stomach and, to a much lesser extent, in the liver. In this study, Fic1 localization and expression during postnatal development was examined in healthy mice.