Differential metabolic effects of glucosamine and N-acetylglucosamine in human articular chondrocytes.

@article{Shikhman2009DifferentialME,
  title={Differential metabolic effects of glucosamine and N-acetylglucosamine in human articular chondrocytes.},
  author={Alexander Shikhman and Diana C. Brinson and J. R. Valbracht and Martin K. Lotz},
  journal={Osteoarthritis and cartilage},
  year={2009},
  volume={17 8},
  pages={
          1022-8
        }
}
OBJECTIVE Aminosugars are commonly used to treat osteoarthritis; however, molecular mechanisms mediating their anti-arthritic activities are still poorly understood. This study analyzes facilitated transport and metabolic effects of glucosamine (GlcN) and N-acetylglucosamine (GlcNAc) in human articular chondrocytes. METHODS Human articular chondrocytes were isolated from knee cartilage. Facilitated transport of glucose, GlcN and GlcNAc was measured by uptake of [3H]2-deoxyglucose, [3H]GlcN… Expand
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References

SHOWING 1-10 OF 43 REFERENCES
Cytokine Regulation of Facilitated Glucose Transport in Human Articular Chondrocytes1
TLDR
Results demonstrate that stimulation of glucose transport represents a component of the chondrocyte response to IL-1β, and does not require phosphoinositide 3-kinase, extracellular signal-related kinase, or c-Jun N-terminal kinase activation. Expand
The lack of effect of glucosamine sulphate on aggrecan mRNA expression and (35)S-sulphate incorporation in bovine primary chondrocytes.
TLDR
Northern blot assay showed that neither hexosamines nor glucosamine sulphate salt stimulated aggrecan and HAS-2 mRNA expression, and Glycosaminoglycan synthesis remained at a control level in the treated cultures, with the exception of mannosamine which inhibited (35)S-sulphate incorporation in low-glucose DMEM treatment. Expand
UDP-sugar metabolism in Swarm rat chondrosarcoma chondrocytes.
UDP-sugars and adenine nucleotides were extracted from freshly isolated chondrocytes and primary cell cultures and analysed by anion-exchange h.p.l.c. The pool sizes of UDP-N-acetylglucosamine,Expand
Effects of [3H]glucosamine concentration on [3H]chondroitin sulphate formation by cultured chondrocytes.
TLDR
It is concluded that the cells have excess capacity to form maximal amounts of GlcN from glucose so that exogenous GlcCN does not stimulate chondroitin sulphate synthesis. Expand
Preferential incorporation of glucosamine into the galactosamine moieties of chondroitin sulfates in articular cartilage explants.
TLDR
The results indicate that GlcN facilitates the production of proteoglycan components that are synthesized through the hexosamine biochemical pathway. Expand
High doses of glucosamine-HCl have detrimental effects on bovine articular cartilage explants cultured in vitro.
TLDR
It is shown that pharmacological doses of glucosamine induce a broad impairment in the metabolic activity of bovine chondrocytes, leading to cell death, and particular attention should be addressed to the experimental model, the doses and the length of treatment. Expand
Effects of glucosamine sulfate on intracellular UDP-hexosamine and UDP-glucuronic acid levels in bovine primary chondrocytes.
TLDR
Physiologically relevant level of GS could not increase the intracellular UDP-HexN and UDP-GlcA levels in bovine primary chondrocyte, while longer-time culture itself appeared to increase the intruder levels. Expand
Distinct pathways regulate facilitated glucose transport in human articular chondrocytes during anabolic and catabolic responses.
TLDR
Anabolic and catabolic stimuli regulate facilitated glucose transport in human articular chondrocytes via different effector and signaling mechanisms, and they have distinct effects on glycolysis. Expand
Stimulation of proteoglycan production by glucosamine sulfate in chondrocytes isolated from human osteoarthritic articular cartilage in vitro.
TLDR
Glucosamine sulfate did not affect DNA synthesis nor coll II production but caused a statistically significant stimulation of PG production by chondrocytes from human osteoarthritic cartilage cultured for up to 12 days in 3-dimensional cultures. Expand
Glucosamine induces insulin resistance in vivo by affecting GLUT 4 translocation in skeletal muscle. Implications for glucose toxicity.
TLDR
Glucosamine is a potent inducer of insulin resistance in vivo by causing (at least in part) a defect intrinsic to GLUT 4 translocation and/or trafficking and a potential role for Glmn to cause glucose-induced insulin resistance (glucose toxicity). Expand
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