Glucosamine

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 …

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.

Objectives To evaluate the associations of regular glucosamine use with all-cause and cause-specific mortality in a large prospective cohort. Methods This population-based prospective cohort study included 495 077 women and men (mean (SD) age, 56.6 (8.1) years) from the UK Biobank study. Participants were recruited from 2006 to 2010 and were followed up through 2018. We evaluated all-cause mortality and mortality due to cardiovascular disease (CVD), cancer, respiratory and digestive disease. HRs and 95% CIs for all-cause and cause-specific mortality were calculated using Cox proportional hazards models with adjustment for potential confounding variables. Results At baseline, 19.1% of the participants reported regular use of glucosamine supplements. During a median follow-up of 8.9 years (IQR 8.3–9.7 years), 19 882 all-cause deaths were recorded, including 3802 CVD deaths, 8090 cancer deaths, 3380 respiratory disease deaths and 1061 digestive disease deaths. In multivariable adjusted analyses, the HRs associated with glucosamine use were 0.85 (95% CI 0.82 to 0.89) for all-cause mortality, 0.82 (95% CI 0.74 to 0.90) for CVD mortality, 0.94 (95% CI 0.88 to 0.99) for cancer mortality, 0.73 (95% CI 0.66 to 0.81) for respiratory mortality and 0.74 (95% CI 0.62 to 0.90) for digestive mortality. The inverse associations of glucosamine use with all-cause mortality seemed to be somewhat stronger among current than non-current smokers (p for interaction=0.00080). Conclusions Regular glucosamine supplementation was associated with lower mortality due to all causes, cancer, CVD, respiratory and digestive diseases.

The present study is performed to investigate the effect of two different glucosamine containing drugs: Drug 1 and Drug 2 (D1 and D2) against CCl4 induced brain damage in male albino rats. Liverin (AM) was employed in the current study as an antioxidant reference drug. CCl4 administration caused a significant elevation in the levels of MDA and NO of brain tissue, in association with a significant decrease in the antioxidant defense system (GSH, SOD and GPX) that indicated the induction of oxidative stress in brain tissue. CCl4 administration induced brain injury as manifested by the obtained changes in neurotransmitter parameter (norepinephrine (NE), Dopamine (DA), Serotonin (5-HT), and Acetylcholinesterase AChE). The tested nutraceuticals and the antioxidant drug displayed a significant improvement against the undue effect of CCl4 via decreasing the brain tissue content of MDA, NO with the elevation of GSH content. Also, the significant increase in SOD and GPX enzymatic activity was obtained when compared to CCL4 group. In addition AM, D1, and D2 have an ameliorative effect on neurotransmitter parameter NE, DA, 5HT, and AChE. Results of this study suggest that both antioxidant drugs and tested nutraceuticals palliate the brain injuries through anti-oxidative effect, with the elimination of the deleterious effect of toxic metabolites of CCl4 on brain tissue.

Purpose: Inflammation in osteoarthritis (OA) has been characterized by infiltration of immune cells and secretion of cytokines into synovial tissues. Also, noradrenaline levels, sympathetic nerve fiber distribution and β2-AR expression in the bone of rats have been associated with subchondral bone loss and increased osteoclast activity. All these data suggest the participation of the adrenergic and immune systems in the development and evolution of OA. However, the relationship among the systemic adrenergic and immune systems activation with the OA progression and treatment response is much less well known.

Glucosamine is a glycosylated amine and a slow-acting symptomatic treatment for osteoarthritis. Some experimental animal studies have shown that glucosamine can cause apoptosis in kidney tubular and mesangial cells as well as overexpression of transforming growth factor β1 (TGF-β1) and connective-ti …

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 …

The derivatives of glucose such as glucosamine (β-D-GlcN) and N-acetyl-D-β-glucosamine (GlcNAc) are significant in several biological systems. D-GlcN …

Background: Glucosamine, chondroitinsulfate are frequently used to prevent further joint degeneration in osteoarthritis (OA). Methylsulfonylmethane (MSM) is a supplement containing organic sulphur and also reported to slow anatomical joint progressivity in the knee OA. The MSM is often combined with glucosamine and chondroitin sulfate. However, there are controversies whether glucosamine-chondroitin sulfate or their combination with methylsulfonylmethane could effectively reduce pain in OA. This study is aimed to compare clinical outcome of glucosamine-chondroitin sulfate (GC), glucosamine-chondroitin sulfate-methylsulfonylmethane (GCM), and placeboin patients with knee osteoarthritis (OA) Kellgren-Lawrence grade I-II. Methods: a double blind, randomized controlled clinical trial was conducted on 147 patients with knee OA Kellgren-Lawrence grade I-II. Patients were allocated by permuted block randomization into three groups: GC (n=49), GCM (n=50), or placebo (n=48) groups. GC group received 1500 mg of glucosamine + 1200 mg of chondroitin sulfate + 500 mg of saccharumlactis; GCM group received 1500 mg of glucosamine + 1200 mg of chondroitin sulfate + 500 mg of MSM; while placebo group received three matching capsules of saccharumlactis. The drugs were administered once daily for 3 consecutive months VAS and WOMAC scores were measured before treatment, then at 4th, 8th and 12th week after treatment. Results: on statistical analysis it was found that at the 12th week, there are significant difference between three treatment groups on the WOMAC score (p=0.03) and on the VAS score (p=0.004). When analyzed between weeks, GCM treatment group was found statistically significant on WOMAC score (p=0.01) and VAS score (p

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Conjugation of D-glucosamine with lipophilic moiety can ease its application in surface modification of liposomes. Interestingly, although D-glucosamine is safe, studies have shed light on “toxic effect” of its conjugates on cancer cells and highlighted its application in targeting glioma. However, understanding the safety of such conjugates for local delivery to the brain is unavailable. Herein, after successful synthesis of D-glucosamine conjugate (GC), the toxicity of functionalized liposome was evaluated both in vitro and in vivo. The study revealed a significant effect on cytotoxicity and apoptosis in vitro as assessed on grade IV-resistant glioma cell lines, SF268, U87MG, using MTT assay and PI staining. Additionally, this effect was not observed on normal human erythrocytes in the hemolysis assay. Furthermore, we demonstrated that GC liposomes were non-toxic to the normal brain tissues of healthy Sprague-Dawley rats. Successful functionalization yielded liposome with uniform particle size, stability, and cellular uptake. With

Background The most important limitations of morphine in pain therapy are its tolerance and dependence. In this study, we evaluated the protective effect of glucosamine against morphine-induced tolerance and dependence in mice. Methods Mice received twice daily morphine (20 mg/kg, s.c.) alone, or along with orally administered glucosamine (500, 1000 and 2000 mg/kg), for 9 continuous days. To assess antinociceptive effect of morphine, percentage of maximal possible effect (%MPE) of animals exposed to thermal stimulus was measured in the hot plate test, 30 min after morphine administration. Test was performed on days 1, 3, 5, 7 and 9. The effect of glucosamine on the naloxone (5 mg/kg, i.p.)-precipitated morphine withdrawal, was also evaluated. Changes in brain gene expression levels of induced nitric oxide synthase (iNOS), enzyme responsible for nitric oxide generation, as well as pro-inflammatory mediator, tumor necrosis alpha (TNF-α) were measured in morphine tolerated animals, as well as after withdrawal by real-time polymerase chain reaction (RT-PCR). Protein content of TNF-α was evaluated via ELISA assay. Results Tolerance to antinociceptive effect of morphine was developed after 7 days of morphine treatment. The concurrent administration of glucosamine (500, 1000 and 2000 mg/kg) with morphine, significantly inhibited tolerance development, on days 7 and 9. In addition, glucosamine ameliorated the naloxone-precipitated opioid withdrawal symptoms (tremor, jumping, teeth chattering, grooming). However, diarrhea was significantly improved only with the dose of 500 mg/kg. Increased mRNA expression of iNOS as well as TNF-α mRNA expression and protein, after both morphine tolerance and withdrawal, were considerably reduced by glucosamine (1000 mg/kg) in the morphine withdrawal animals. Conclusion These data support the utility of glucosamine in attenuating both tolerance to nociceptive effects of morphine as well as withdrawal-induced behavioral profile. Anti-oxidant and anti-inflammatory effects are responsible, at least in part, for the protective effects of this drug.

Aim The aim was to study whether oral glucosamine hydrochloride (GlcN.HCl) or mucopolysaccharide protein (MucoP) has a structure-modifying effect on an anterior cruciate ligament transection (ACLT) ...

Background: Glucosamine sulphate (GS) is essential in the biosynthesis of glycolipids, glycoproteins, glycosaminoglycans (GAGs), hyaluronate, and proteoglycans. Connective tissues primarily contain collagen and proteoglycans and play an important role in skin ageing. Objective: The objectives were to assess ex vivo the impact of GS on skin ageing p

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.