Glucosamine

The present study aimed to evaluate the effect of N‑acetyl‑glucosamine (GlcNAc) on the joint health of healthy individuals without arthritic symptoms. A randomized double‑blind placebo‑controlled clinical trial was performed to investigate the effect of oral administration of a GlcNAc‑containing test supplement (low dose, 500 mg/day and high dose, 1,000 mg/day) on cartilage metabolism in healthy individuals with a mean age of 48.6±1.3 years (range, 23‑64 years) by analyzing the ratio of type II collagen degradation to type II collagen synthesis using type II collagen degradation (C2C) and synthesis (PIICP) markers. The results indicated that the changes in C2C/PIICP ratios from the baseline were suppressed in the treated with low and high doses of GlcNAc, compared with the placebo group at week 16 during intervention. To further elucidate the effect of GlcNAc, subjects with impaired cartilage metabolism were evaluated. Notably, the changes in the C2C/PIICP ratios were markedly suppressed in the groups treated with low and high doses of GlcNAc at week 16. Finally, to exclude the effect of heavy body weight on joint loading, subjects weighing

Background: To evaluate the chondroprotective action of an N-acetyl-glucosamine (GlcNAc)-containing supplement on the joint health of healthy individuals without symptoms of arthritis, we conducted a randomized double-blind placebo-controlled clinical trial.  Methods: Subjects (n=100, 51.3 ± 1.0 years (mean ± SE)) without symptoms of arthritis were randomly assigned to receive a 1000 mg GlcNAc-containing diet (GlcNAc group) or a placebo diet (placebo group) once a day for 16 weeks, and the effect on the cartilage metabolism was evaluated by analyzing the ratio of type II collagen degradation to synthesis using type II collagen degradation (C2C) and synthesis (PIICP) markers. Results: The results indicated that the changes in the C2C/PIICP ratios from the baseline were slightly suppressed in the GlcNAc group compared with those in the placebo group at weeks 16 during the intervention and 4 weeks after the intervention. However, there was no significant difference between the two groups. To make the effect of GlcNAc even more clear, the subjects with joint loading and impaired cartilage metabolism were evaluated. Interestingly, the changes in the C2C/PIICP ratios from the baseline were significantly suppressed in the GlcNAc group compared with the placebo group at weeks 16 during the intervention and 4 weeks after the intervention. Moreover, test supplement-related adverse events were not essentially observed during and after the intervention. Conclusions: These observations suggest that the oral administration of GlcNAc at a dose of 1000 mg/day exerts a chondroprotective action on the healthy individuals by lowering the C2C/PIICP ratio, which indicates relative reduction of type II collagen degradation and increase of type II collagen synthesis, without apparent adverse effect.  Key words: N-acetyl-glucosamine, biomarker, cartilage metabolism, joint health

Background: To evaluate the chondroprotective action of an N-acetyl-glucosamine (GlcNAc)-containing supplement on the joint health of healthy individuals without symptoms of arthritis, we conducted a randomized double-blind placebo-controlled clinical trial.  Methods: Subjects (n=100, 51.3 ± 1.0 years (mean ± SE)) without symptoms of arthritis were randomly assigned to receive a 1000 mg GlcNAc-containing diet (GlcNAc group) or a placebo diet (placebo group) once a day for 16 weeks, and the effect on the cartilage metabolism was evaluated by analyzing the ratio of type II collagen degradation to synthesis using type II collagen degradation (C2C) and synthesis (PIICP) markers. Results: The results indicated that the changes in the C2C/PIICP ratios from the baseline were slightly suppressed in the GlcNAc group compared with those in the placebo group at weeks 16 during the intervention and 4 weeks after the intervention. However, there was no significant difference between the two groups. To make the effect of GlcNAc even more clear, the subjects with joint loading and impaired cartilage metabolism were evaluated. Interestingly, the changes in the C2C/PIICP ratios from the baseline were significantly suppressed in the GlcNAc group compared with the placebo group at weeks 16 during the intervention and 4 weeks after the intervention. Moreover, test supplement-related adverse events were not essentially observed during and after the intervention. Conclusions: These observations suggest that the oral administration of GlcNAc at a dose of 1000 mg/day exerts a chondroprotective action on the healthy individuals by lowering the C2C/PIICP ratio, which indicates relative reduction of type II collagen degradation and increase of type II collagen synthesis, without apparent adverse effect.  Key words: N-acetyl-glucosamine, biomarker, cartilage metabolism, joint health

What is glucosamine? Glucosamine is a polysaccharide that naturally occurs in cartilaginous joint tissues and is involved in protein and lipid synthesis. […]

What is glucosamine? Glucosamine is a polysaccharide that naturally occurs in cartilaginous joint tissues and is involved in protein and lipid synthesis. […]

An in-depth scientific review of glucosamine and chondroitin - including their background, evidenced-based health benefits, risks, side effects and more!

In Alzheimer’s disease (AD), amyloid-β (Aβ) oligomers are considered key mediators of synaptic dysfunction and cognitive impairment. These unstable intermediate Aβ species can interfere with different cellular organelles, leading to neuronal cell death, through the formation of Ca2+-permeable membrane pores, impairment in the levels of acetylcholine neurotransmitters, increased insulin resistance, promotion of pro-inflammatory cascades, among others. Based on a series of evidences that indicate the key role of glycosaminoglycans (GAGs) in amyloid plaque formation, we evaluated the capacity of four monosaccharides, i.e., glucosamine (GlcN), N-acetyl glucosamine (GlcNAc), glucosamine-6-sulfate (GlcN6S), and glucosamine-6-phosphate (GlcN6P), to reduce the Aβ-mediated pathological hallmarks. The tested monosaccharides, in particular, GlcN6S and GlcN6P, were able to interact with Aβ aggregates, reducing neuronal cell death, Aβ-mediated damage to the cellular membrane, acetylcholinesterase activity, insulin resistance, and pro-inflammation levels.

I read with interest the paper by Li et al 1 reporting the association of regular glucosamine use with lower mortality. The authors report significantly lower all-cause mortality HR 0.85 (95% CI 0.82 to 0.89), cardiovascular mortality HR 0.82 (95% CI 0.74 to 0.90), cancer mortality HR 0.94 (95% CI 0.88 to 0.99), respiratory mortality HR 0.73 (95% CI 0.66 to 0.81) and digestive mortality HR 0.74 (95% CI 0.62 to 0.90). The magnitude of the reported reduction in mortality is striking, as is the consistency across major disease categories. The results reported by the authors are consistent with other prior epidemiological studies looking at glucosamine and mortality.2–4 The biological plausibility for glucosamine having such pronounced causative effects …

Plantar fasciitis is the most common cause of the plantar heel pain. Its main features are a pain, tenderness mostly on the medial aspect of the calcaneum near the sole of heel. There are many conservative methods for treatment of the lantar fasciitis which include rest, massage, night splints, orthoses, injections, cast NSAID, shock wave therapy. The glucosamine is one of the nutritional product which has a good anti- properties and is already in use for arthritis knee. Depending on anti-inflammatory analgesic property can also be used in planter fasciitis. In this study 17 patients were studied after giving fixed dose of 1200 mg of glucosamine. The evaluation was done on linkert pain score. The p-value in studied group was

Cancer stem cells (CSCs) are a subpopulation of cancer cells responsible for tumor maintenance and relapse due to their ability to resist various anticancer effects. Owing to the resistance of CSCs to the effects of targeted therapy, an alternative strategy that targets post‑translational glycosylation may be an improved approach to treat cancer as it disrupts multiple coordinated signaling that maintains the stemness of CSCs. Glucosamine acts as an anticancer agent possibly by inhibiting N‑linked glycosylation. The aim of the present study was to investigate the effect of glucosamine on the stemness of breast CSCs, which is regulated by signal transducer and activator of transcription 3 (STAT3) signaling. Human aldehyde dehydrogenase‑positive (ALDH+) breast CSCs and MCF7 cells were treated with various concentrations (0.25, 1 or 4 mM) of glucosamine for 24 h. Subsequently, cell viability was determined by performing a trypan blue exclusion assay, pluripotency gene [ALDH 1 family member A1 (ALDH1A1), octamer‑binding transcription factor 4 (OCT‑4), and Krüppel‑like factor 4 (KLF4)] expression was determined using the reverse transcription‑quantitative polymerase chain reaction, and STAT3 and phosphorylated STAT3 (pSTAT3) levels were determined by performing western blot analysis. Furthermore, the number of mammosphere‑forming units (MFUs) in ALDH+ breast CSCs and MCF7 cells was determined. It was determined that glucosamine treatment decreased the viability of ALDH+ breast CSCs. Glucosamine treatment also decreased the stemness of ALDH+ breast CSCs and MCF7 cells, as indicated by decreased ALDH1A1, OCT‑4 and KLF4 expression level, and a decreased number of MFUs. This effect of glucosamine may be associated with a decreased pSTAT3/STAT3 ratio, indicating that glucosamine inhibited STAT3 activation; therefore, the results of the present study indicated that glucosamine treatment may be an improved approach to target the stemness of CSCs.

Background: Glucosamine hydrochloride (GlcN·HCl) has been shown to inhibit cell growth and matrix synthesis, but not with N-acetyl-glucosamine (GlcNAc) supplementation. This effect might be related to an inhibition of critical growth factors (GF), or to a different metabolization of the two glucosamine derivatives. The aim of the present study was to evaluate the synergy between GlcN·HCl, GlcNAc, and GF on proliferation and cartilage matrix synthesis. Method: Bovine chondrocytes were cultivated in monolayers for 48 h and in three-dimensional (3D) chitosan scaffolds for 30 days in perfusion bioreactors. Serum-free (SF) medium was supplemented with either growth factors (GF) TGF-β (5 ng mL−1) and IGF-I (10 ng mL−1), GlcN·HCl or GlcNAc at 1mM each or both. Six groups were compared according to medium supplementation: (a) SF control; (b) SF + GlcN·HCl; (c) SF + GlcNAc; (d) SF + GF; (e) SF + GF + GlcN·HCl; and (f) SF + GF + GlcNAc. Cell proliferation, proteoglycan, collagen I (COL1), and collagen II (COL2) synthesis were evaluated. Results: The two glucosamines showed opposite effects in monolayer culture: GlcN·HCl significantly reduced proliferation and GlcNAc significantly augmented cellular metabolism. In the 30 days 3D culture, the GlcN·HCl added to GF stimulated cell proliferation more than when compared to GF only, but the proteoglycan synthesis was smaller than GF. However, GlcNAc added to GF improved the cell proliferation and proteoglycan synthesis more than when compared to GF and GF/GlcN·HCl. The synthesis of COL1 and COL2 was observed in all groups containing GF. Conclusion: GlcN·HCl and GlcNAc increased cell growth and stimulated COL2 synthesis in long-time 3D culture. However, only GlcNAc added to GF improved proteoglycan synthesis.

Glucosamine hydrochloride (GH) and chondroitin sulfate (CS) are commonly used for the treatment of osteoarthritis (OA). The aim of this study was to assess their effects, alone and in combination, on preventing aggrecan degradation and inflammation in ...

Background Transforming growth factor (TGF) family members play important roles in the regulation of corneal integrity, and the pathogenesis of corneal fibrosis. Currently, there are no effective agents targeting TGF-β signaling to diminish corneal fibrosis. Glucosamine (GlcN), which is widely used in the treatment of osteoarthritis, abrogates the morphologic effects of TGF-β2 on retinal pigmented epithelial cells in a mouse disease model. Here, we sought to determine whether GlcN would exert beneficial effects against TGF-β1-induced corneal fibrosis. Methods In human corneal fibroblasts (HCFs) treated with GlcN, the expression of Krüppel-like factor 4 (KLF4) and its downstream signaling effects were determined in the presence and absence of TGF-β1 using immunoblot analysis. We further explored GlcN inhibition of fibroblast-to-myofibroblast differentiation via KLF4 siRNA. The effect of cycloheximide on KLF4 protein levels with or without GlcN administration was assessed to determine whether GlcN affects the stability of the KLF4 protein. Results In HCFs, GlcN induced the expression of KLF4, which regulated the maturation and maintenance of the ocular surface. GlcN partially suppressed the TGF-β1-induced expression of alpha-smooth muscle actin (α-SMA) and reduced the collagen contraction capacity in HCFs, suggesting a decrease in fibroblast-to-myofibroblast differentiation. This effect appeared to be mediated through suppression of Smad2 phosphorylation and ERK-dependent signaling. The levels of KLF4 mRNA were increased by GlcN and decreased by TGF-β1 and the TGF-β1-induced α-SMA mRNA expression was upregulated when the KLF4 gene was silenced. GlcN also appeared to stabilize the KLF4 protein, reducing its turnover in corneal fibroblasts. Conclusion These findings shed light on a novel mechanism by which GlcN suppresses TGF-β1-induced fibroblast-to-myofibroblast differentiation through the upregulation of KLF4 expression. Current strategies for treating corneal fibrosis were not effective. Elevating KLF4 levels through the use of GlcN might provide an effective alternative to alleviate the development and progression of corneal fibrosis.

The aim of the current study was to investigate the effects of glucosamine (GlcN) on septic lethality and sepsis-induced inflammation using animal models of mice and zebrafish. GlcN pretreatment improved survival in the cecal ligation and puncture (CLP)-induced sepsis mouse model and attenuated lipo …

Glucosamine is an essential substrate for N-linked protein glycosylation. However, elevated levels of glucosamine can induce endoplasmic reticulum (ER) stress. Glucosamine-induced ER stress has bee...

Glucosamine is an essential substrate for N-linked protein glycosylation. However, elevated levels of glucosamine can induce endoplasmic reticulum (ER) stress. Glucosamine-induced ER stress has bee...

The NLRP3 inflammasome promotes the pathogenesis of metabolic, neurodegenerative and infectious diseases. Increasing evidences show that the NLRP3 inflammasome is a promising therapeutic target in inflammatory diseases. Glucosamine is widely used as a dietary supplement to promote the health of cartilage tissue and is expected to exert anti-inflammatory activity in joint inflammation, which is a nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasome-associated complication. Here, we investigated whether GlcN inhibits the NLRP3 inflammasome and dissected the underlying molecular mechanisms. We found that GlcN suppressed the NLRP3 inflammasome in mouse and human macrophages. A mechanistic study revealed that GlcN inhibited the expression of NLRP3 and IL-1β precursor by reducing reactive oxygen species generation and NF-κB activation in lipopolysaccharide-activated macrophages. GlcN also suppressed mitochondrial reactive oxygen species generation and mitochondrial integrity loss in NLRP3-activated macrophages. Additionally, GlcN disrupted NLRP3 inflammasome assembly by inhibiting NLRP3 binding to PKR, NEK7 and ASC. Furthermore, oral administration of GlcN reduced peritoneal neutrophils influx and lavage fluids concentrations of IL-1β, IL-6 MCP-1 and TNF-α in uric acid crystal-injected mice. These results indicated that GlcN might be a novel dietary supplement for the amelioration of NLRP3 inflammasome-associated complications.

Glucosamine (GlcN) is a naturally occurring derivative of glucose and an over-the-counter food additive. However, the mechanism underlying GlcN action on cells is unknown. In this study, we investigated the effect of GlcN on natural killer (NK) cells. We demonstrate that GlcN affects NK-92 cell cytotoxicity by altering the distribution of cathepsin C, a cysteine protease required for granzyme processing in cytotoxic granules. The relocation of cathepsin C due to GlcN was shown to be accompanied by a decrease in the intracellular enzyme activity and its extracellular secretion. Similarly, the relocation of endosomal aspartic cathepsin E was observed. Furthermore, we elucidated that repositioning of cathepsin C is a consequence of altered signaling pathways of cytotoxic granule movement. The inhibition of phosphorylation upstream and downstream of ERK by GlcN disturbed the polarized release of cytotoxic vesicles. Considerable changes in the ERK phosphorylation dynamics, but not in those of p38 kinase or JNK, were observed in the IL2-activated NK-92 cells. We found decreased phosphorylation of the transcription factor FOXO1 and simultaneous prolonged phosphorylation of ERK as well as its nuclear translocation. Additionally, a protein downstream of the ERK phosphorylation cascade, paxillin, was less phosphorylated, resulting in a diffuse distribution of cytotoxic granules. Taken together, our results suggest that dietary GlcN affects signaling pathway activation of NK-92 immune cells.

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Glucosamine (GlcN), a dietary supplement widely utilized to promote joint health and effective in the treatment of osteoarthritis, is an effective macroautophagy/autophagy activator in vitro and in vivo. Previous studies have shown that autophagy is required for hepatitis B virus (HBV) …

Glucosamine is effective in the treatment of osteoarthritis; however, its effect on osteoporosis remains unclear. Decreased activity of osteoblasts is the main cause of osteoporosis. Here, we examined the effects of glucosamine on osteoblasts. The potential underlying mechanisms were explored. The r …

Europe PMC is an archive of life sciences journal literature.

Background We assessed whether local anaesthetics caused inhibition of proteoglycan metabolism in human articular cartilage and whether the addition of Glucosamine sulphate could prevent or allow recovery from this adverse effect on articular cartilage metabolism. Methods Cartilage explants obtained from 13 femoral heads from fracture neck of femur patients (average age 80 years, 10 female) were exposed to either 1% Lidocaine, 2% Lidocaine, 0.25% Bupivacaine, 0.5% Bupivacaine, 0.5% Levo-bupivacaine or a control solution (M199 culture medium). Glucosamine-6-Sulphate was added during or 1 h after exposure to 0.5% Bupivacaine to assess its protective and reparative effects. After exposure, the explants were incubated in culture medium containing radio labelled 35-sulphate and uptake was measured after 16 h to give an assessment of proteoglycan metabolism. Results The reduction in 35-S uptake compared to control was 65% for 1% Lidocaine (p < 0.001), 79% for 2% Lidocaine (p < 0.001), 61% for 0.25% Bupivacaine (p < 0.001), 85% for 0.5% Bupivacaine (p < 0.001) and 77% for 0.5% Levobupivacaine (p < 0.001). Glucosamine was able to protect the articular cartilage by reducing the inhibition of proteoglycan metabolism of 0.5% Bupivacaine from 85 to 30% (p < 0.001). When added after 0.5% Bupivacaine exposure, Glucosamine allowed some recovery with inhibition of metabolism to 70% (p = 0.004). Conclusion Our results showed that all local anaesthetic solutions inhibited proteoglycan metabolism in articular cartilage and the addition of Glucosamine was able to reduce the inhibition of metabolism caused by 0.5% Bupivacaine. Intra-articular injection of local anaesthetics requires careful consideration of risks and benefits.

Obesity is associated with metabolic disorders. Fibroblast growth factor 21 (FGF21) has been recognized as important in metabolism. Glucosamine (GLN) …

Glucosamine (GlcN), a natural amino sugar in human body, was reported to exhibit anticancer activity against some tumors. In the present study, we eva…

(2020). Glucosamine Reverses P-Glycoprotein-Mediated Multidrug Resistance in the Daunorubicin-Resistant Human Gastric Cancer Cells. Nutrition and Cancer: Vol. 72, No. 3, pp. 522-527.

Author summary Cryptococcal meningitis claims half a million lives each year. There is no clinically available vaccine and the current antifungal therapies have serious limitations. Thus identifying cryptococcal specific programs that can be targeted for antifungal or vaccine development is of great value. We have shown previously that switching from the yeast to the hypha form drastically attenuates/abolishes cryptococcal virulence. Cryptococcal cells in the filamentous form also trigger host immune responses that can protect the host from a subsequent lethal challenge. However, self-filamentation is rarely observed in serotype A isolates that are responsible for the vast majority of cryptococcosis cases. In this study, we found that glucosamine stimulated self-filamentation in genetically distinct strains of the Cryptococcus species complex, including the most commonly used serotype A reference strain H99. We demonstrated that filamentation elicited by glucosamine did not depend on the pheromone pathway, but it requires the calcineurin transcription factor Crz1. Glucosamine promotes nuclear translocation of Crz1, which is positively controlled by the phosphatase calcineurin and is suppressed by the HOG pathway. These findings raise the possibility of manipulating genetic pathways controlling fungal morphogenesis against diseases caused by the Cryptococcus species complex.