Article Text

  1. T. N. Pham,
  2. R. H. Scofield
  1. University of Oklahoma, Oklahoma City


Summary Glucosamine is a widely used drug as a disease-modifying treatment by improving resilience and decreasing radiographic progression in osteoarthritic joints. In animal studies, both in vitro and in vivo studies with glucosamine suggest increase insulin resistance by affecting insulin receptor phosphorylation and decrease translocation of Glut 1 and Glut 4 translocation to plasma membranes. We undertook this study to determine whether insulin resistance occurs in nondiabetic subjects after six weeks of 1500 mg of glucosamine a day.

Methods Before and after completion of six weeks of glucosamine, thirty-two subjects had evaluation for parameters of insulin resistance such as fasting insulin and glucose, HDL, LDL, and triglycerides as well as large and small artery elasticity by such and as such. Serum values for insulin and glucose were used to calculate log HOMA and QUICKI. Exclusion criteria included a history of diabetes, polycystic ovarian disease, or subjects on medication known to cause insulin resistance. Student's paired t-test was used to evaluate parameters in subjects before and directly after glucosamine use, and means are reported.

Results The log HOMA, a direct measure of insulin resistance, showed a significant rise after 6 weeks of glucosamine with mean values before and after of 0.29 ± 0.37 and 0.36 ± 0.36 (p = .008). In addition, QUICKI, which is inversely correlated with insulin resistance, demonstrated a significant fall (0.637 ± 0.136 versus 0.606 ± 0.12, p = .017). The serum triglycerides (mg/dL) increased from 117 ± 54.6 at baseline to 137 ± 80.9 at the end of 6 weeks of glucosamine, but this difference did not reach statistical significance (p = .201). Meanwhile, there was no statistical change or trend in any other lipid measurement, including HDL-C (41.9 ± 11.8 mg/dL versus 43.3 ± 11.2 mg/dL, p = .319), LDL-C (99.1 ± 28 versus 98.2 ± 24.1 mg/dL, p = .738). We measured arterial elasticity as mL/mg HGX100 with an HDI sonogram of the radial artery. Small artery elasticity worsened, falling from 7.21 ± 3.6 to 6.60 ± 3.16 (p = .118) after six weeks of glucosamine, as did large artery elasticity (17.7 ± 5.14 versus 16.4 ± 4.22, p = .085).

Conclusion After 6 weeks of glucosamine treatment in nondiabetic subjects, indices such as log HOMA and QUICKI demonstrate significantly increased insulin resistance, while measures of arterial elasticity and serum triglycerides lean toward statistical significance. In conclusion, glucosamine, in doses shown to be effective in osteoarthritis that is widely prescribed and taken, causes insulin resistance in humans.

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