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At least 235 records · Page 13Linked to original sources

PubMed2004

Polyvalent dendrimer glucosamine conjugates prevent scar tissue formation.

Dendrimers are hyperbranched macromolecules that can be chemically synthesized to have precise structural characteristics. We used anionic, polyamidoamine, generation 3.5 dendrimers to make novel water-soluble conjugates of D(+)-glucosamine and D(+)-glucosamine 6-sulfate with immuno-modulatory and antiangiogenic properties respectively. Dendrimer glucosamine inhibited Toll-like receptor 4-mediated lipopolysaccharide induced synthesis of pro-inflammatory chemokines (MIP-1 alpha, MIP-1 beta, IL-8) and cytokines (TNF-alpha, IL-1 beta, IL-6) from human dendritic cells and macrophages but allowed upregulation of the costimulatory molecules CD25, CD80, CD83 and CD86. Dendrimer glucosamine 6-sulfate blocked fibroblast growth factor-2 mediated endothelial cell proliferation and neoangiogenesis in human Matrigel and placental angiogenesis assays. When dendrimer glucosamine and dendrimer glucosamine 6-sulfate were used together in a validated and clinically relevant rabbit model of scar tissue formation after glaucoma filtration surgery, they increased the long-term success of the surgery from 30% to 80% (P = 0.029). We conclude that synthetically engineered macromolecules such as the dendrimers described here can be tailored to have defined immuno-modulatory and antiangiogenic properties, and they can be used synergistically to prevent scar tissue formation.

Animals↗

PubMed1970

The influence of insulin on the metabolism of glucosamine in the isolated rat diaphragm muscle.

1. The influence of insulin on the metabolism of [1-(14)C]glucosamine by diaphragm muscle from normal rats and rats rendered diabetic with streptozotocin has been studied. 2. The glucosamine was converted into glucosamine 1-phosphate, glucosamine 6-phosphate, glycogen, lactate and small amounts of other unidentified intermediates. 3. Insulin increased the incorporation of (14)C into glycogen in both the normal and diabetic muscle, but did not increase the formation of the glucosamine phosphate esters. 4. The (14)C content in the glycogen was present partly as glucose and partly as glucosamine; there was significantly more [(14)C]glucose in the glycogen of the diabetic muscle than in that of the normal muscle.

Animals↗

PubMed1995

Presence of N-unsubstituted glucosamine units in native heparan sulfate revealed by a monoclonal antibody.

Immunohistochemical application of antibodies against heparan sulfate proteoglycan core protein and heparitinase-digested heparan sulfate stubs showed the presence of heparan sulfate proteoglycan in all basement membranes of the rat kidney. However, a monoclonal antibody (JM-403) against native heparan sulfate (van den Born, J., van den Heuvel, L. P. W. J., Bakker, M. A. H., Veerkamp, J. H., Assmann, K. J. M., and Berden, J. H. M. (1992) Kidney Int. 41, 115-123) largely failed to stain tubular basement membranes, suggesting the presence of heparan sulfate chains lacking the specific JM-403 epitope. Heparan sulfate preparations from various sources differed markedly with regard to JM-403 binding, as demonstrated by liquid phase inhibition in enzyme-linked immunosorbent assay, the interaction decreasing with increasing sulfate contents of the polysaccharide. Mapping of the JM-403 epitope indicated that it was dominated by one or more N-unsubstituted glucosamine unit(s), since treatments that destroyed or altered the structure of such units in heparan sulfate preparations (cleavage at N-unsubstituted glucosamine units with HNO2 at pH 3.9 and N-acetylation with acetic anhydride, respectively), abolished antibody binding. Conversely, immunoreactivity could be induced in a (D-glucuronyl-1,4-N-acetyl-D-glucosaminyl-1,4) polysaccharide by the generation of N-unsubstituted glucosamine N-unsubstituted glucosamine in a JM-403-binding heparan sulfate (preparation HS-II from human aorta) was demonstrated by an approximately 3-fold reduction in molecular size following HNO2 (pH 3.9) treatment. Further characterization of the epitope recognized by JM-403, based on enzyme-linked immunosorbent assay inhibition tests with chemically/enzymatically modified polysaccharides, indicated that one or more N-sulfated glucosamine units are invariable present, whereas L-iduronic acid and O-sulfate residues appear to inhibit JM-403 reactivity. It is concluded that the epitope contains one or more N-unsubstituted glucosamine and D-glucuronic acid units and is located in a region of the heparan sulfate chain composed of mixed N-sulfated and N-acetylated disaccharide units.

Animals↗

PubMed2000

In vivo chondroprotection and metabolic synergy of glucosamine and chondroitin sulfate.

Supplements of glucosamine hydrochloride, low molecular weight chondroitin sulfate, and manganese ascorbate were tested separately and in combination for their ability to retard progression of cartilage degeneration in a rabbit instability model of osteoarthrosis. Computerized quantitative histologic evaluation of safranin O stained sections of the medial femoral condyles measured the grade and extent of tissue involvement of lesions. Severe lesions (Mankin grade greater than 7) were absent in all animals supplemented with a dietary mixture of glucosamine, chondroitin sulfate, and manganese ascorbate. Total linear involvement (mm of lesioned surface) and total grade (mean grade x number of lesions per animal) were reduced significantly in animals given the combination compared with controls (59% and 74% respectively). Animals supplemented with glucosamine, chondroitin sulfate, or manganese ascorbate alone had less moderate and severe tissue involvement than controls but not to the extent of the combined group. In vitro, a combination of glucosamine hydrochloride and chondroitin sulfate acted synergistically in stimulating glycosaminoglycan synthesis (96.6%). Chondroitin sulfate and manganese ascorbate but not glucosamine were effective in inhibiting degradative enzyme activity. These data suggest that the disease modifying effect (the ability to retard progression of cartilage degeneration) of a mixture of glucosamine, chondroitin sulfate, and manganese ascorbate is more efficacious than either agent alone.

Animals↗

PubMed1975

Changes in glucosamine and galactosamine levels during conidial germination in Neurospora crassa.

The levels of glucosamine and galactosamine were determined in conidia, germinating conidia, and vegetative mycelia of Neurospora crassa. In the vegetative mycelia about 90% of the amino sugars were shown to be components of the cell wall. The remaining 10% of the amino sugars were tentatively identified as the nucleotide sugars uridine diphospho-2-acetamido-2-deoxy-D-glucose and uridine diphospho-2-acetamido-2-deoxy-D-galactose. Conidia and vegetative mycelia contained about the same levels of glucosamine. During the first 9 h after the initiation of germination, the total glucosamine content had increased 3.1-fold, whereas the residual dry weight of the culture had increased 7.7-fold. This led to a drop in the glucosamine concentration from 100 mumol/g of residual dry weight to 42 mumol/g. During this time, all of the conidia had germinated and the surface area of the new germ tubes had increased to 10 times that of the conidia. Either germ tubes were initially produced without glucosamine-containing polymers, or these polymers (probably chitin) were deposited only at low densities in the germ tube cell walls. The chitin precursor uridine diphospho-2-acetamido-2-deoxy-D-glucose was present at all times during conidial germination. Conida contained very low levels of galactosamine. During germination, galactosamine could not be detected until the culture had reached a cell density of about 0.6 mg of residual dry weight per ml of growth medium. This was observed regardless of the time required to reach this cell density or the fold increase in dry weight. The accumulation of galactosamine-containing polymers does not appear to be necessary for germ tube formation. The levels of soluble galactosamine (uridine diphospho-2-actamido-2-deoxy-D-galatose) were very low in conidia and increased during germination at the same time that galactosamine appeared in the cellular polymers. In addition, under certain culture conditions, the appearance of galactosamine and the increase in the glucosamine concentration occurred simultaneously.

Autoanalysis↗

PubMed2006

Effects of oral glucosamine sulphate on serum glucose and insulin during an oral glucose tolerance test of subjects with osteoarthritis.

BACKGROUND: and objective: Glucosamine is suggested to affect glucose transport and insulin resistance. The effects of oral glucosamine on serum glucose and insulin levels at the initiation and throughout the duration of a 3-h oral glucose tolerance test were examined. METHODS: Sera from 16 patients with osteoarthritis, but with no other diagnosed medical condition who had fasted overnight, were obtained every 15-30 min during the 3 h of continued fasting and during the 3 h after ingestion of 75 g of glucose with or without ingestion of 1500 mg of glucosamine sulphate. Glucose was analysed by high-performance liquid chromatography using a Metrohm-Peak 817 Bioscan, and the area under the curve (AUC) for glucose was calculated. Insulin was measured by radioimmunoassay every 30 min for 2 h. RESULTS: Three participants who were found to have previously undiagnosed abnormalities of glucose tolerance demonstrated significant (p = 0.04) incremental elevations in glucose levels after ingestion of glucosamine sulphate. The other 13 participants also had mean incremental elevations that were not significant (p = 0.20). Glucosamine sulphate ingestion had no effect on insulin levels. CONCLUSION: The results suggest that glucosamine ingestion may affect glucose levels and consequent glucose uptake in patients who have untreated diabetes or glucose intolerance.

Adult↗

PubMed2000

Randomized, controlled trial of glucosamine for treating osteoarthritis of the knee.

OBJECTIVE: To determine the effectiveness of glucosamine in reducing pain from osteoarthritis of the knee. DESIGN: Randomized, double-blind parallel trial of glucosamine 500 mg three times daily or a placebo for 2 months. SETTING: Veterans Affairs Medical Center, Prescott, AZ. PARTICIPANTS: Ninety-eight patients aged 34 to 81 being treated for osteoarthritis of the knee. MAIN OUTCOME MEASURES: Pain intensity both at rest and while walking as assessed by a visual analog scale at baseline and after 30 and 60 days of treatment. RESULTS: Forty-nine patients were randomly allocated to each group. There was no statistical difference between the two groups in scores on the visual analog scale at 30 days for resting (mean [SD] score placebo group 3.5 [2.7] vs 3.3 [2.4] glucosamine group, P = 0.66) or walking (5.1 [2.6] vs 5.3 [2.4], P = 0.69); there was also no difference at 60 days for resting (3.4 [2.5] vs 3.2 [2.5], P = 0.81) or walking (4.9 [2.2] vs 4.9 [2.8], P = 0.90). There was also no statistical difference between groups in the mean change from baseline in scores on the visual analog scale (mean [SD] change for walking at 60 days placebo group -1.5 [2.5] vs glucosamine group -1.4 [3.0], P = 0.77). Two participants taking glucosamine and 4 taking placebo withdrew from the study due to adverse side effects (P = 0.67). CONCLUSION: Glucosamine was no better than placebo in reducing pain from osteoarthritis of the knee in this group of patients.

Aged↗

PubMed2002

Chitosan and D-glucosamine induce expression of Th1 cytokine genes in porcine spleen cells.

Chitosan, a polymer of D-glucosamine, is a polysaccharide derived from the chitin found in the exoskeleton of shellfish, such as shrimp or crabs. The effects of chitosan has been recognized that chitosan-fed farm animals demonstrated higher weight gains but less incidence of diseases than the unfed ones. However, these beneficial effects has not been elucidated clearly. In this study, we examined the modulatory effect of chitosan and D-glucosamine on the expression of porcine cytokines in vitro. Porcine spleen cells were cultured in the presence of chitosan and D-glucosamine, and the effects of chitosan on the cytokine mRNA expression were evaluated. Expressions of IL-2 and IFN-gamma were increased in the chitosan-treated porcine spleen cells. Expressed cytokines in the D-glucosamine-treated cells were IL-2, IFN-gamma, and IL-12 p40 subunit. In particular, IFN-gamma was expressed more efficiently, and D-glucosamine was more effective for expressing the cytokine gene. These results suggest chitosan as well as D-glucosamine could induce the expression of cytokines as Th1 subset such as IL-2, IFN-gamma.

Animals↗

PubMed2002

Glucosamine therapy compared to ibuprofen for joint pain.

To determine the effectiveness of oral glucosamine with ibuprofen for the relief of joint pain in osteoarthritis a mini-review (Griffiths, 2002) of double-blind randomized controlled trials comparing the two was undertaken. The population was adult patients diagnosed with osteoarthritis at any site. The outcome was arthritic pain reduction. Searches on Medline, Embase, AMED, the Cochrane Library and the Merck index identified four trials. Of these, two studies were obtainable and were included in the review. Both compared 1.2 g ibuprofen daily with 1.5 g glucosamine sulphate daily, in three divided doses. The combined number of participants in the studies was 218. The results of these studies showed glucosamine to be of similar efficacy to ibuprofen. The conclusion is that glucosamine is effective in relieving joint pain associated with osteoarthritis. Glucosamine's pain-relieving effects may be due to its cartilage-rebuilding properties; these disease-modifying effects are not seen with simple analgesics and are of particular benefit. In practice glucosamine can be used as an alternative to anti-inflammatory drugs and analgesics or as a useful adjunct to standard analgesic therapy.

Arthralgia↗

PubMed1987

An autoradiographic study using [3H]glucosamine of gonadotrophin regulation of proteoglycan and glycoprotein synthesis in developing mouse follicles.

Autoradiography of serial sections of ovaries of immature mice was used, after an injection of [3H]glucosamine, to follow the migration of newly synthesized macromolecules into preantral follicles during the period of treatment with PMSG and hCG. [3H]Glucosamine was injected at the same time as the PMSG or 2-h before the time of autopsy. PMSG stimulated a modest uptake of [3H]glucosamine into the zona pellucida of preantral follicles. However, the in-vivo synthesis of labelled macromolecules increased substantially during the period of hCG stimulation, especially in those mice in which the label was injected at the same time as the PMSG. After both short and longer term exposure to [3H]glucosamine, the maximum uptake of label in preantral follicles occurred 4-8 h after the injection of hCG, indicating that hCG rather than PMSG probably exerts the greatest control over the uptake and incorporation of [3H]glucosamine into the zona pellucida and oocyte of preantral follicles. It is suggested that [3H]glucosamine is largely incorporated into non-sulphated glycosaminoglycans.

Animals↗

PubMed2004

Cumulus expansion and glucose utilisation by bovine cumulus-oocyte complexes during in vitro maturation: the influence of glucosamine and follicle-stimulating hormone.

Glucose is an important metabolite and its presence during in vitro oocyte maturation (IVM) can have profound effects on the oocyte's developmental capacity. We have demonstrated that glucose uptake increases over a 24 h IVM period, with most accounted for as l-lactate production. However, as maturation proceeds, l-lactate production remains constant, suggesting an alternative role for glucose metabolism. We hypothesised that in the latter stages of oocyte maturation, glucose not accounted for by l-lactate production is utilised for FSH-stimulated extracellular matrix (ECM) synthesis. To examine precursor utilisation for synthesis of ECM, bovine cumulus-oocyte complexes (COCs) were matured in +/- FSH and/or glucosamine (an alternative substrate of matrix components). Measurements included COC diameters, glucose consumption and l-lactate production in spent media and [U-(14)C]glucose incorporation into ECM. FSH significantly stimulated both diameter and glucose consumption during 20-24 h maturation compared with unstimulated complexes, although co-incubation with glucosamine and FSH decreased total glucose consumption 1.7-fold compared with FSH alone (P < 0.05). Furthermore, there was a linear relationship between glucose and l-lactate metabolism in the presence of glucosamine, suggesting that the majority of glucose was being utilised for l-lactate production via glycolysis. In the presence of glucosamine, twofold less [U-(14)C]glucose was incorporated into matrix compared with COCs cultured without glucosamine. These results support the hypothesis that there is a link between glucose and glucosamine uptake in FSH-stimulated ECM synthesis. Furthermore, glucose has multiple fates within the COC during maturation and levels of utilisation are dependent on the composition of the maturation environment.

Animals↗

PubMed2004

Comparison of inhibitory effects of glucosamine and mannosamine on bovine articular cartilage degradation in vitro.

OBJECTIVE: To compare the inhibitory effects of glucosamine and mannosamine on articular cartilage degradation and the effects on chondrocyte viability in vitro. SAMPLE POPULATION: Bovine articular cartilage explants. PROCEDURES: Explants were cultured in commercial medium for 48 hours. Cartilage was exposed to medium containing 10% fetal bovine serum, 10 microg 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 < or = 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.

Animals↗

PubMed2003

The effect of exogenous glucosamine hydrochloride on the proteoglycan concentration of the articular disc of the rabbit temporomandibular joint.

AIMS: To test the effect of glucosamine hydrochloride (glucosamine-HCl) on the proteoglycan (PG) concentration of the articular disc of non-arthritic temporomandibular joints (TMJs) in rabbits. METHODS: Twenty-four of 48 New Zealand white 10- to 12-week-old male rabbits (2.2 kg average) were injected with the irritant chymopapain in the knee joint. Both groups of 24 rabbits were divided into 3 groups of 8 animals. The rabbits were fed a control diet or a diet supplemented with glucosamine-HCl incorporated at a level to provide 20 mg/kg (approximating the recommended dose 500 mg/tid/70 kg man) or 100 mg/kg, for 8 weeks. Sulfated glycosaminoglycans (GAGs) were assayed in protease K digests of the TMJ articular disc by dimethylmethylene blue method to quantify PG concentration. The groups were compared with 2-way analysis of variance. RESULTS: Glucosamine-HCl did not cause a significant change in the PG concentration of the TMJ articular disc (P > .8). There was also no detectable effect of chymopapain injection to the knee joint on the TMJ (P > .07) and no interaction between glucosamine-HCl treatment and chymopapain injection (P > .3). CONCLUSION: Glucosamine-HCl has no effect on PG concentration of the articular disc of non-arthritic TMJ in rabbits.

Analysis of Variance↗

PubMed2005

Current concepts in the therapeutic management of osteoarthritis with glucosamine.

Over the last 10 years, several studies have investigated the ability of glucosamine sulfate to improve the symptoms (pain and function) and to delay the structural progression of osteoarthritis. There is now a large, convergent body of evidence that glucosamine sulfate, given at a daily oral dose of 1,500 mg, is able to significantly reduce the symptoms of osteoarthritis in the lower limbs and spine. This effect is usually seen with a minimal time for the onset of significant action - around 2 weeks. A similar dose of glucosamine sulfate has also been shown, in two independent studies, to prevent the joint space narrowing observed at the femorotibial compartment in patients with mild to moderate knee osteoarthritis. This effect, which is not affected by the radiographic technique used for the assessment of joint space width, also translated into a 50% reduction in the incidence of osteoarthritis-related surgery of the lower limbs during a 5-year period following the withdrawal of the treatment. There is a high degree of consistency in the literature showing that when glucosamine sulfate is used for the treatment of osteoarthritis, an efficacious response with minimum side effects can be expected. Since some discrepancies have been described between the results of studies performed with a patent-protected formulation of glucosamine sulfate distributed as a drug and those having used glucosamine preparations purchased from global suppliers, packaged, and sold over-the-counter as nutritional supplements (not regulated as drugs and with some potential issues concerning the reliability of their content), caution should be used when extrapolating conclusive results obtained with prescription drugs to over-the-counter or food supplements.

Drug Prescriptions↗

PubMed2006

The role of glucosamine, chondroitin and thymoquinone on the viability and proliferation of a HTB-93 rheumatoid arthritis cell model.

Glucosamine (GS), chondroitin (CD), and thymoquinone (TQ) are the complementary medicines under investigation in this study. Glucosamine is a naturally occurring glycoaminoglycan that contributes to the development of proteoglycans needed for the development of cartilage development and regeneration. Chondroitin is also a naturally occurring glycoaminoglycans (GAG) that seems to support the efforts of glucosamine as well as provide chondroprotection while serving as a 'water magnet' within the joint matrix. Thymoquinone is derived naturally from the black seed plant that is extremely popular within Middle Eastern countries. Its benefits are multiple, including both antioxidant and anti-inflammatory properties. These products were administered to HTB-93 synovial cells and cell viability, damage, and alterations in morphology were analyzed after 72 hours. Preliminary results revealed that chondroitin increased cell number in the high treatment group with increased nitric oxide production and decreased glutathione content compared to the control, glucosamine, and TMQ. Decreased glutathione levels were seen in the medium and high doses of both glucosamine and chondroitin. Increased levels of glutathione were seen with increasing TMQ, without changes in cell numbers or nitric oxide. The data indicates that medium and high doses of glucosamine and chondroitin may be cytotoxic to HTB-93 synovial cells.

Arthritis, Rheumatoid↗

PubMedDate not supplied

[The influence of experimental therapy on the dynamics of endogenous glucosamine content in laboratory animals with nephropathy].

The effects of glucosamine hydrochloride, glucosamine sulfate, N-acetylglucosamine, glucosamine pentaacetate, and combinations of glucosamine hydrochloride and N-acetylglucosamine with diclofenac sodium on the endogenous glucosamine (aminosugar) content in the blood and kidney of rats with experimental nephropathy have been studied. The development of inflammatory and destructive processes in kidneys is accompanied by an increase in the aminosugar content in the blood serum and the corresponding decrease in renal tissues. This fact can be used as a nonspecific diagnostic criterion for the level of kidney damage and for the efficacy of pharmacotherapy. Normalization of these indices in the case of successful therapy was observed, which was most pronounced upon the administration of glucosamine hydrochloride, N-acetylglucosamine, and their combinations with diclofenac sodium.

Acetylglucosamine↗

PubMed1989

The distribution of glucosamine in mammalian glycogen from different species, organs and tissues.

The reasons for the occurrence of trace amounts of glucosamine in animal liver glycogens have been explored. Human liver glycogen is now shown to contain this amino sugar. Galactosamine, known to be the source of the incorporated glucosamine, is found to give rise to glucosamine in glycogen when administered orally, or as the N-acetyl derivative. The rabbit can also incorporate glucosamine into kidney glycogen but not into glycogen in heart or skeletal muscle. These experiments led to the discovery that glucosamine is incorporated into rabbit liver glycogen in such a way that there is intermolecular heterogeneity in the content of glucosamine, suggesting that there exists more than one pool of liver glycogen.

Animals↗

PubMed1986

Pharmacokinetics of glucosamine in the dog and in man.

The pharmacokinetics, organ distribution, metabolism and excretion of glucosamine were studied in the dog giving uniformly labelled [14C]-glucosamine (sulfate), i.v. or orally, in single doses. Immediately after i.v. administration, the radioactivity in plasma is due to glucosamine, and freely diffuses into organs and tissues. This radioactivity disappears quickly from plasma (initial t1/2 = 13 min, terminal t1/2 = 118 min). After 30-60 min the radioactivity in plasma is no longer due to glucosamine, but is incorporated into alpha- and beta-globulins. The protein-incorporated radioactivity is found already 20-30 min after i.v. administration, reaches a peak after 8 h and then slowly disappears, with a t1/2 = 2.9 days. Of the administered radioactivity, more than 34% is excreted in the urine, mainly as glucosamine, and 1.7% is excreted in the feces. Radioactivity is excreted also as [14C]-CO2 in the expired air. The radioactivity, after i.v. administration, diffuses rapidly from blood into the body. Some organs show an active uptake of radioactivity, e.g. the liver and the kidney. Other tissues, such as the articular cartilage, also have an active uptake. In most other organs the radioactivity found can be explained by passive diffusion processes from plasma. After oral administration of a single dose of [14C]-glucosamine the radioactivity is quickly and almost completely absorbed from the gastrointestinal tract. The pattern of disappearance, metabolic transformation, tissue distribution and excretion of the radioactivity are consistent with those found after i.v. administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗