Analyze Diet
Osteoarthritis and cartilage2000; 8(6); 444-451; doi: 10.1053/joca.1999.0320

The effects of glucosamine derivatives on equine articular cartilage degradation in explant culture.

Abstract: To determine whether glucosamine-3-sulfate, glucose-3-sulfate (control) and N-acetyl glucosamine inhibit experimentally induced degradation of equine articular cartilage explants similar to glucosamine HCl. Methods: Articular cartilage was obtained from the antebrachio-carpal and middle joints of horses (2-8 years old) killed for reasons unrelated to lameness. Cartilage discs were harvested from the weight-bearing region of the articular surface and cultured. Media were exchanged daily and the recovered media stored at 4 degrees C. On days 1 and 2 lipopolysaccharide (LPS, 10 microg/ml) was added to induce cartilage degradation. To evaluate the effects of different sources of glucosamine (on an equal molar basis), varying concentrations of glucosamine HCl (0.25, 2.5, or 25 mg/ml), glucosamine-3-sulfate (0.304, 3.04, or 30.4 mg/ml), or N-acetyl-glucosamine (0.256, 2.56, or 25.6 mg/ml) were added to the cultures. The glucose-3-sulfate control was added at 0.3075, 3.075 or 30.75 mg/ml. Nitric oxide and proteoglycan released into conditioned media and tissue proteoglycan synthesis and total tissue PG content were measured as indicators of cartilage metabolism. Results: Glucosamine-3-sulfate consistently inhibited cartilage degradation in a manner similar to glucosamine HCl, while the effects of N-acetyl-glucosamine were highly variable and did not inhibit cartilage degradation. Glucose-3-sulfate did not inhibit cartilage degradation. Conclusions: Our results indicate that glucosamine sulfate also has the potential to prevent or reduce articular cartilage degradation similar to glucosamine HCl in vitro. The amine group at the carbon-2 position appears important for the effectiveness of the glucosamine derivative. The therapeutic value of N-acetyl-glucosamine remains questionable.
Publication Date: 2000-11-09 PubMed ID: 11069729DOI: 10.1053/joca.1999.0320Google Scholar: Lookup
The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research investigates the effects of different glucosamine derivatives on the degradation of horse’s articular cartilage. The findings suggest that glucosamine-3-sulfate can potentially prevent or reduce cartilage degradation similar to glucosamine HCl.

Introduction and Methodology

  • The study aimed to determine if glucosamine-3-sulfate, glucose-3-sulfate (used as a control), and N-acetyl glucosamine can inhibit the degradation of equine articular cartilage explants similar to glucosamine HCl, a commonly used supplement for maintaining joint health.
  • Articular cartilage was obtained from the joints of horses aged between 2-8 years, which had been killed for unrelated reasons. The weight-bearing regions of the articular surface were specifically chosen for the study.
  • The harvested cartilage pieces were then cultured in a lab. The media in which the cartilages were grown was changed daily.
  • To induce cartilage degradation in this laboratory setting, lipopolysaccharide (LPS) was added on the first and second days of the experiment.
  • For comparison, different concentrations of glucosamine HCl, glucosamine-3-sulfate, N-acetyl-glucosamine, and the glucose-3-sulfate control were added to the cultures. The amounts were matched on an equal molar basis.
  • The researchers studied the release of nitric oxide and proteoglycan into the media, and the synthesis of tissue proteoglycan and total tissue PG content as indications of cartilage metabolism.

Results

  • The outcomes showed that glucosamine-3-sulfate consistently inhibited cartilage degradation similar to glucosamine HCl.
  • The effects of N-acetyl-glucosamine, on the other hand, were highly variable and did not inhibit cartilage degradation in a consistent manner. Thus, it’s usefulness is uncertain.
  • Glucose-3-sulfate, the control, as anticipated, did not inhibit cartilage degradation.

Conclusion

  • The findings indicate that glucosamine sulfate also has the potential to prevent or reduce articular cartilage degradation, just like glucosamine HCl.
  • The study further highlights the importance of the amine group at the carbon-2 position in the efficacy of glucosamine derivatives.
  • However, the therapeutic value of N-acetyl-glucosamine remains questionable, considering the inconsistent responses noted in this research.

Cite This Article

APA
Fenton JI, Chlebek-Brown KA, Peters TL, Caron JP, Orth MW. (2000). The effects of glucosamine derivatives on equine articular cartilage degradation in explant culture. Osteoarthritis Cartilage, 8(6), 444-451. https://doi.org/10.1053/joca.1999.0320

Publication

ISSN: 1063-4584
NlmUniqueID: 9305697
Country: England
Language: English
Volume: 8
Issue: 6
Pages: 444-451

Researcher Affiliations

Fenton, J I
  • Department of Animal Science, Michigan State University, East Lansing, Michigan 48824, USA.
Chlebek-Brown, K A
    Peters, T L
      Caron, J P
        Orth, M W

          MeSH Terms

          • Acetylglucosamine / pharmacology
          • Animals
          • Cartilage, Articular / drug effects
          • Cartilage, Articular / metabolism
          • Culture Techniques
          • Dose-Response Relationship, Drug
          • Glucosamine / pharmacology
          • Glucose / pharmacology
          • Horses / metabolism
          • Lipopolysaccharides / pharmacology
          • Nitric Oxide / metabolism
          • Proteoglycans / metabolism

          Citations

          This article has been cited 7 times.
          1. Pizzolatti ALA, Gaudig F, Seitz D, Roesler CRM, Salmoria GV. Glucosamine Hydrochloride and N-Acetylglucosamine Influence the Response of Bovine Chondrocytes to TGF-β3 and IGF in Monolayer and Three-Dimensional Tissue Culture. Tissue Eng Regen Med 2018 Dec;15(6):781-791.
            doi: 10.1007/s13770-018-0150-xpubmed: 30603596google scholar: lookup
          2. Gulihar A, Shaunak S, Novak PL, Vinayakam P, Dhinsa B, Taylor G. Glucosamine reduces the inhibition of proteoglycan metabolism caused by local anaesthetic solution in human articular cartilage: an in vitro study. J Exp Orthop 2017 Nov 13;4(1):37.
            doi: 10.1186/s40634-017-0106-4pubmed: 29134408google scholar: lookup
          3. Chang NJ, Lin YT, Lin CC, Wang HC, Hsu HC, Yeh ML. The repair of full-thickness articular cartilage defect using intra-articular administration of N-acetyl-D-glucosamine in the rabbit knee: randomized controlled trial. Biomed Eng Online 2015 Nov 18;14:105.
            doi: 10.1186/s12938-015-0100-ypubmed: 26582033google scholar: lookup
          4. Phitak T, Pothacharoen P, Kongtawelert P. Comparison of glucose derivatives effects on cartilage degradation. BMC Musculoskelet Disord 2010 Jul 15;11:162.
            doi: 10.1186/1471-2474-11-162pubmed: 20630114google scholar: lookup
          5. Uitterlinden EJ, Koevoet JL, Verkoelen CF, Bierma-Zeinstra SM, Jahr H, Weinans H, Verhaar JA, van Osch GJ. Glucosamine increases hyaluronic acid production in human osteoarthritic synovium explants. BMC Musculoskelet Disord 2008 Sep 11;9:120.
            doi: 10.1186/1471-2474-9-120pubmed: 18786270google scholar: lookup
          6. Silva RM, Elvira C, Mano JF, San Román J, Reis RL. Influence of beta-radiation sterilisation in properties of new chitosan/soybean protein isolate membranes for guided bone regeneration. J Mater Sci Mater Med 2004 Apr;15(4):523-8.
          7. Wang Y, Huang Y, Zhou P, Lu S, Lin J, Wen G, Shi X, Guo Y. Effects of dietary glucosamine sulfate sodium on early laying performance and eggshell quality of laying hens. Poult Sci 2024 Sep;103(9):103982.
            doi: 10.1016/j.psj.2024.103982pubmed: 39013294google scholar: lookup