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Glucosamine as its chloride or sulphate salt is now in widespread over‐the‐counter use for the treatment of osteoarthritis, ostensibly by stimulating or stabilizing cartilage chondroitin sulphate. Clinical trials have, however, provided equivocal results concerning its effectiveness,1,2,3 and measurements of serum4 and plasma5 glucosamine levels after ingestion indicate that circulating glucosamine levels are probably too low to have any direct effect on cartilage.
Suggestions have been made that the sulphate of glucosamine sulphate might have a positive clinical effect on cartilage as a result of an increase in circulating levels after its ingestion.6,7 This may be particularly pertinent because we previously described8 a 9.3% mean decrease of sulphate levels after three hours of fasting by 14 experimental subjects, with a doubling of this mean decrease to 18.9% by the concomitant ingestion of 75 g glucose. In addition, we have described an effect of glucosamine sulphate ingestion by these subjects on glucose and insulin levels when 75 g glucose was ingested.9 Results were in contrast to other investigations10 that have indicated little or no effect when glucose was ingested the day after the ingestion of glucosamine rather than ingestion at the same time.
We have now examined the reciprocal effects of glucose ingestion on serum sulphate and glucosamine levels during a three hour period after an overnight fast. Methods, materials, subjects, study protocol, serum collection and analyses are detailed in previous publications.4,8,9
Sulphate levels during three hours after overnight fasting with no additional ingestion, with 0 time ingestion of 75 g glucose, 0 time ingestion of 1500 g glucosamine sulphate, and 0 time ingestion of 75 g glucose plus 1500 g glucosamine sulphate are shown in fig 1A1A.. The ingestion of glucosamine sulphate without glucose restored mean sulphate levels to slightly above baseline at each time interval, in contrast to the decreases with fasting when no glucosamine sulphate was ingested as previously reported.8 The simultaneous ingestion of glucose and glucosamine sulphate compared with glucose alone resulted in restoration to somewhat less than baseline for the first two hours and to slightly higher afterwards. The total amount of sulphate ingested (325 mg equal to 3.25 mmol) is consistent with the incremental amounts that were found in serum.
Mean glucosamine levels (fig 1B1B)) demonstrated a delay in appearance and were higher and still climbing when glucose was ingested along with glucosamine sulphate, probably reaching still higher levels if serum had been taken at later times. Two subjects had later samples obtained, however, showing a drop towards baseline at five hours and baseline at eight hours. The delay in the increase in glucosamine levels when ingested with glucose rather than without glucose is consistent with the competitive inhibition of glucosamine by glucose for transport from the gastrointestinal tract. Furthermore, higher serum levels might be expected because glucose would competitively inhibit the uptake of glucosamine into the liver, thus allowing a higher concentration of glucosamine to enter the peripheral circulation. We do not believe that the minimal raising or extending glucosamine levels would be of significant therapeutic benefit.
Support was provided by the Medical Research Service of the Department of Veterans Affairs, a grant to J.E.S. by the Arthritis Foundation, and by the Tufts University General Clinical Research Center, funded by the Division of Research Resources of the National Institutes of Health (NIH) under grant no. MO1‐RR00054, US Department of Health and Human Services, NIH and Agency for Healthcare Research and Quality, Ruth L. Kirschstein National Research Service Award (T‐32).