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

The aim of the stuy was to observe and analyze the effect of glucosamine hydrochloride tablets on patients with cervical spondylosis. This study was conducted on 130 patients diagnosed with cervical spondylosis who were treated in our hospital. The time period was from June 2015 to December 2017. Th …

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. […]

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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

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.

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 ...

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.

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 Glucosamine hydrochloride, a natural biopolymer present in the daily diet, has various biological activities including antitumour properties and protective effects against pathogens. Early studies showed that daily administration of a derivative of glucosamine induced proliferation of leukemia cells and prolonged overall survival in mice; importantly, no toxicity was associated with the glucosamine treatment. However, the potential mechanism of the antitumour effect is unknown. This study aimed to investigate the inhibitory mechanism and effect of glucosamine on human gastric carcinoma cells in vitro. Methods Gastric carcinoma MKN-45 cells were exposed to 0, 100, 500 and 1000 µg/mL glucosamine hydrochloride for 72 hours, and then the viability and proliferation of gastric carcinoma cells in vitro was measured using the MTT (3-(4.5-dimethylthiazol-2-yl)-2.5-diphenyltetrazolium bromide) assay. Quantitative gene expression of MMP-2 and -3 was determined by real-time polymerase chain reaction. Protein level was analyzed using an enzyme-linked immunosorbent assay (ELISA). Results Glucosamine hydrochloride has a significant inhibitory antitumour effect on MKN-45 cells in vitro. The cell viability of MKN-45 cells treated with different concentrations of glucosamine hydrochloride rose continuously from 24 to 72 hours compared with the untreated control. MKN-45 cells were inhibited by 54% by 500 µg/mL glucosamine hydrochloride and by 85% by 1000 µg/mL glucosamine hydrochloride. Administration of 500 µg/mL glucosamine hydrochloride resulted in a significant decrease in MMP-2 and MMP-3 expression of about 79% and 70%, respectively, in MKN-45 cells. Conclusions In this study, we showed that the antitumour activity of glucosamine hydrochloride significantly suppresses MKN-45 cells in vitro. This effect was shown by inhibitory gene expression of MMP-2 and -3. Acknowledgments This research was financially supported by Zhuhai College of Jilin University.

Background: Osteoarthritis (OA) is a degenerative disease with complex underling mechanisms 1–3. The interactions among several factors make the study of the disease very complex and often lead to different treatment, i.e. surgical or conservative, decisions for subjects clinically and radiographically similar. Recent explorations performed at the body level pointed out that macro-factors, like overweight or gait, can influence the development of the disease 4. The number of related factors is high, and they are very likely to interact with each other. However, the literature lacks randomized and balanced studies to verify such effects of multiple factors 5. Objectives: The aim of this work was to develop a multifactorial analysis to explore whether and how gait functionality and dynamics can be related to treatment decision. Methods: A multifactorial analysis of gait dynamics in OA subjects was developed. 81 OA subjects, graded 2-3 in KL, were selected based on 4 clinical factors: Gender (male – female), Age (60-67 – 68-75), BMI (25–29.9 – 30+) and Treatment (total knee replacement (TKR) – conservative treatment). Gait analysis was performed using 8 cameras BTS Smart-DX 700, 1.5 Mpixels 250 fps and 2 force plates BTS P-6000 500 Hz sampling (BTS S.p.A., Milan, Italy). Helen Hayes marker protocol with medial markers was used for the study. Each volunteer was asked to perform a minimum of 5 valid gait sequences. Functionality and dynamics parameters were measured. Functionality : Velocity of gait and the time needed to perform a gait cycle were computed. Dynamics: The reaction forces and torques at the ankles, knees and hips were computed through inverse dynamic analyses. Analysis of variance was performed for the four factors described among the functionality and dynamics parameters. Results: The multifactorial analysis showed that functionality values are more subjective to the studied factors than the dynamics ones. Functionality seems to be directly related to the clinical treatment. Patients who selected TKR needed more time to make a step, spent more time in double stand position and walked slower (p

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

Osteoarthritis is a chronic degenerative joint disease causing pain and disability. Glucosamine sulphate is a well known oral supplement for its treatment. The present pioneering study provides an overview of the accentuated transdermal delivery of glucosamine sulphate through the optimized gel formulation w

Rheumatoid arthritis (RA) is an autoimmune disorder that affects the joint synovium. Anserine is a functional dipeptide containing methylhistidine and β-alanine, and is present in the brain and skeletal muscle of birds and mammals. Glucosamine is an amino sugar used in the synthesis of glycosylated proteins and lipids. We evaluated the effects of anserine and glucosamine on RA. Rats were assigned into the control group, RA group, anserine group (1 mg/kg), glucosamine group (200 mg/kg), or anserine plus glucosamine group (anserine, 1 mg/kg + glucosamine, 200 mg/kg). Treatment was continued for 45 consecutive days and was administered orally. The serum levels of catalase, glutathione peroxidase (Gpx), superoxide dismutase (SOD), reduced glutathione (GSH), lipid peroxidation, uric acid, nitric oxide, ceruloplasmin, zinc, copper, prostaglandin E2 (PGE2), matrix metalloproteinase (MMP)-3, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 were assayed. The mRNA and protein levels of nuclear factor (NF)-κB and inducible nitric oxide synthase (iNOS) in synovial tissue were also determined. Anserine plus glucosamine significantly increased the catalase, SOD, Gpx, GSH, and zinc levels compared to the control, anserine, and glucosamine groups. Also, anserine plus glucosamine significantly reduced the PGE2, MMP-3, TNF-α, IL-1β, and IL-6 levels compared to the control, anserine, and glucosamine groups. Furthermore, anserine plus glucosamine significantly reduced the mRNA and protein levels of NF-κB and iNOS compared to the control, anserine, and glucosamine groups. Therefore, supplementation of anserine plus glucosamine shows therapeutic potential for RA.

Lung cancer is the most common cause of cancer‑associated mortality worldwide, and glucosamine has the potential to exhibit antitumor activity. To reveal its anti‑lung cancer mechanism, the present study investigated the effect of glucosamine on the transcriptional activity of forkhead box O (FOXO)1 …

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 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 …

Background Renal cell carcinoma (RCC) is one of the most common types of cancer in urological system worldwide. Recently, the anticancer role of Glucosamine has been studied in many types of cancer. The aim of this study was to investigate the effects of Glucosamine on RCC. Methods The effects of Glucosamine on RCC cell proliferation and apoptosis were investigated by MTT assay and Annexin V-FITC Apoptosis assay, respectively in vitro. Cell cycle was detected by flow cytometry after treatment with Glucosamine. Protein levels of several cell cycle associated markers were examined by Western Blot. Results Our data showed that Glucosamine significantly inhibited the proliferation of renal cancer 786-O and Caki-1 cells in a dose-dependent manner. Besides, Glucosamine treatment resulted in cell cycle arrest at G0/G1 phase in both cell lines. Meanwhile, the expression of several regulators that contribute to G1/S phased transition, such as Cyclin D1, CDK4 and CDK6, were significantly down-regulated with the up-regulation of cell cycle inhibitors, p21 and p53, after treatment with glucosamine. However, the apoptosis rate of RCC cells was down-regulated when treatment with Glucosamine at 1 mM and 5 mM, while up-regulated at 10 mM. Conclusions Our findings indicated that Glucosamine inhibited the proliferation of RCC cells by promoting cell cycle arrest at G0/G1 phase, but not promoting apoptosis. The present results suggested that Glucosamine might be a potential therapeutic agent in RCC treatment in the future.

Glucosamine (GlcN), also known as aminosaccharide, is an important functional monosaccharide and the first amino monosaccharide to be identified as a hydroxyl group of glucose substituted by amino ...

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Objective To prospectively assess the association of habitual glucosamine use with risk of cardiovascular disease (CVD) events. Design Prospective cohort study. Setting UK Biobank. Participants 466 039 participants without CVD at baseline who completed a questionnaire on supplement use, which included glucosamine. These participants were enrolled from 2006 to 2010 and were followed up to 2016. Main outcome measures Incident CVD events, including CVD death, coronary heart disease, and stroke. Results During a median follow-up of seven years, there were 10 204 incident CVD events, 3060 CVD deaths, 5745 coronary heart disease events, and 3263 stroke events. After adjustment for age, sex, body mass index, race, lifestyle factors, dietary intakes, drug use, and other supplement use, glucosamine use was associated with a significantly lower risk of total CVD events (hazard ratio 0.85, 95% confidence interval 0.80 to 0.90), CVD death (0.78, 0.70 to 0.87), coronary heart disease (0.82, 0.76 to 0.88), and stroke (0.91, 0.83 to 1.00). Conclusion Habitual use of glucosamine supplement to relieve osteoarthritis pain might also be related to lower risks of CVD events.