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. 2016 Mar 1;20(5):769–781. doi: 10.1111/jcmm.12807

Figure 2.

Figure 2

A schematic model illustrating the effect of glucose, thiamet‐G and insulin on O‐GlcNAcylation and phosphorylation of signalling molecules during chondrogenesis. High glucose up‐regulates p38 and down‐regulates ERK activity through PKCα, priming stimulating chondrogenesis by increasing the expression of adhesion molecules. Insulin and glucose/thiamet‐G stimulate chondrogenic differentiation by inducing O‐GlcNAcylation and phosphorylation and of signalling molecules, including MAPK, p38 and ERK1/2. Insulin induces O‐GlcNAcylation and phosphorylation of Akt, while high glucose and thiamet‐G simply induce Akt O‐GlcNAcylation. Then activated‐Akt stimulates proteoglycan synthesis in chondrocytes.