Objective—To determine the effects of orally administered
glucosamine on concentrations of markers of
bone and cartilage metabolism in Standardbred horses
during race training.
Animals—Twenty 16- to 20-month-old Standardbreds
beginning race training.
Procedure—Horses were randomly assigned to 2
groups. One group received glucosamine hydrochloride
(4 g, PO, q 12 h), and the second (control) group
received glucose (4 g, PO, q 12 h). Serum samples
were obtained prior to onset of the study (baseline)
and at regular intervals for 48 weeks for determination
of concentrations of keratan sulfate (KS), osteocalcin
(OC), and pyridinoline crosslinks (PYD).
Results—Osteocalcin concentrations changed significantly
with time; mean serum concentrations were
significantly higher than baseline values for samples
obtained at 24 to 48 weeks after onset of the study.
Although a significant effect of time was observed for
mean concentration of KS, concentrations did not differ
significantly from baseline values at any time during
the study when groups were analyzed separately.
However, pooled analysis revealed significant increases
of mean serum KS concentration at weeks 24 and
30. Significant changes in serum PYD concentrations
were not detected. Oral administration of glucosamine
did not significantly affect serum concentrations
of any of the markers.
Conclusions and Clinical Relevance—Increased
serum OC in clinically normal Standardbreds during
race training may reflect bone formation that accompanies
adaptive remodeling of the appendicular skeleton.
For these experimental conditions, glucosamine did
not appear to exert a detectable influence on serum
concentrations of these 3 markers of connective tissue
metabolism. (Am J Vet Res 2002;63:1106–1110)
Procedures—Explants were cultured in commercial
medium for 48 hours. Cartilage was exposed to medium
containing 10% fetal bovine serum, 10 µg of
lipopolysaccharide/mL, and 0.5, 1.0, 2.5, 5.0, and
10.0 mg of glucosamine or mannosamine/mL for 24
hours. Nitric oxide (NO) production (nitrite concentration)
and proteoglycan (PG) release (PG concentration)
in media were measured . Cartilage extracts
were analyzed via zymography to detect gelatinolytic
activity. At the end of the experiment, explants were
assessed for chondrocyte viability.
Results—Addition of lipopolysaccharide resulted in
increased NO production and PG release, but no
increase in gelatinolytic activity, compared with controls.
Glucosamine and mannosamine at concentrations
as low as 0.5 mg/mL inhibited NO production.
Glucosamine inhibited PG release at a minimum concentration
of 1.0 mg/mL, whereas mannosamine
inhibited PG release at a concentration of 0.5 mg/mL.
Concentrations of glucosamine ≤ 5.0 mg/mL did not
adversely affect chondrocyte viability; however, at a
concentration of 10.0 mg/mL, cell death was evident.
Mannosamine had a toxic effect at a concentration of
5.0 mg/mL and was associated with pronounced
chondrocyte death at a concentration of 10.0 mg/mL.
Conclusions and Clinical Relevance—Glucosamine
and mannosamine inhibit selected indices of bovine
articular cartilage degradation at concentrations that
do not affect chondrocyte viability. The potential for
cytotoxic effects at higher concentrations underscores
the importance of establishing appropriate
dosage regimens for these aminomonosaccharides.
(Am J Vet Res 2004;65:1440–1445)