Articular cartilage is an avascular, non-insulin sensitive tissue which utilizes glucose as the main energy source, precursor for glycosaminoglycan synthesis and regulator of gene expression. Facilitated glucose transport represents the first rate-limiting step in glucose metabolism. Previously, we demonstrated that glucose transport in chondrocytes is regulated by proinflammatory cytokines via upregulation of GLUT mRNA and protein expression. The objective of the present study was to determine differences in molecular mechanisms regulating glucose transport in chondrocytes stimulated with the anabolic growth factor TGFb1 versus the catabolic and proinflammatory cytokine IL-1b. Both TGFb1 and IL-1b accelerate glucose transport in chondrocytes. Although both IL-1b and TGFb1 enhance glucose transport in chondrocytes to a similar magnitude, IL-1b induces significantly higher levels of lactate. TGFb1-stimulated glucose transport is not associated with increased expression or membrane incorporation of GLUT1, 3, 6, 8 and 10, and depends on PKC and ERK activation. In contrast, IL-1b-stimulated glucose transport is accompanied by increased expression and membrane incorporation of GLUT1 and 6, and depends upon activation of PKC and p38 MAP kinase. In conclusion, anabolic and catabolic stimuli regulate facilitated glucose transport in human articular chondrocytes via different effector and signaling mechanisms, and have distinct effects on glycolysis.