This 2024 study grew human cartilage cells in glucose levels from the normal blood range to the high range. At 10 mM against 4 mM, cells from osteoarthritic cartilage made more MMP13 and ADAMTS5 at 18.9% oxygen, but not at 1% oxygen. Cells from macroscopically normal cartilage did not show the rise.
Researchers took chondrocytes from osteoarthritic and from macroscopically normal human cartilage and kept them in 4, 6, 8 or 10 mM glucose for 24 hours, at either 18.9% or 1% oxygen. They measured glucose use, the glucose transporter GLUT1, MMP13, ADAMTS5 and RUNX2, a gene regulator that controls all three, using enzyme assays, RT-qPCR and Western blots.
At 18.9% oxygen, osteoarthritic chondrocytes in 10 mM glucose used more glucose, had more GLUT1 protein, and made more MMP13 and ADAMTS5, as RNA and as protein, than in 4 mM. Their RUNX2 protein, though not its RNA, was also higher. Normal chondrocytes showed none of these increases. At 1% oxygen, neither RUNX2 nor the two enzymes rose with glucose. The authors suggest high blood sugar may speed cartilage breakdown in the oxygen-rich surface layer in people whose high blood sugar is poorly controlled.
The cells were exposed for 24 hours in a dish, and the abstract does not give the number of donors. Glucose in culture medium is not the same as blood sugar reaching cartilage inside a joint. The link to blood sugar in people is the authors' suggestion, not something this study measured in people.
It gives a cell-level route from blood sugar to cartilage breakdown: more glucose, more RUNX2 protein, more MMP13 and ADAMTS5. It also shows the effect depends on oxygen and on whether the cells already come from worn cartilage, so healthy-looking cartilage cells did not respond the same way.
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