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Journal articles on the topic 'Glucosamine'

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Published: 4 June 2021
Last updated: 28 July 2024

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1

Gening, Marina L., Yury E. Tsvetkov, Denis V. Titov, Alexey G. Gerbst, Olga N. Yudina, Alexey A. Grachev, Alexander S. Shashkov, et al. "Linear and cyclic oligo-β-(1→6)-D-glucosamines: Synthesis, conformations, and applications for design of a vaccine and oligodentate glycoconjugates." Pure and Applied Chemistry 85, no. 9 (September 1, 2013): 1879–91. http://dx.doi.org/10.1351/pac-con-12-09-06.

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Poly-β-(1→6)-N-acetyl-D-glucosamine is an exopolysaccharide secreted by numerous pathogenic bacteria, includingStaphylococcus aureus,Escherichia coli,Yersinia pestis,Bordetella pertussis,Acinetobacter baumannii,Burkholderiaspp., and others. A convergent approach was developed for the synthesis of oligosaccharide fragments consisting of 5, 7, 9, and 11 glucosamine orN-acetylglucosamine units and for the preparation of five nona-β-(1→6)-D-glucosamines with variousN-acetylation patterns. Penta- and nona-β‑(1→6)-D-glucosamines conjugated to protein carriers through a specially developed sulfhydryl linker proved to be highly immunogenic in mice and rabbits and elicited antibodies that mediated opsonic killing of multiple strains ofS. aureus(including methicillin-resistantS. aureus, MRSA) andE. coli, and protected againstS. aureusskin abscesses and lethalE. coliandB. cenocepaciaperitonitis. These findings provide a basis for the construction of a unique semisynthetic vaccine against multiple bacterial targets. Conformational studies by means of special NMR experiments and computer modeling revealed that the oligo-β-(1→6)-D-glucosamine chain exists mostly in a helix-like conformation, where the terminal monosaccharides are arranged close to each other. Owing to this feature, oligoglucosamines consisting of 2 to 7 residues easily form products of cycloglycosylation. Cyclooligo-β-(1→6)-D-glucosamines represent a new family of functionalized cyclic oligosaccharides. Owing to their molecular architectonics, these compounds are convenient scaffolds for the design of conjugates with defined valency, symmetry, flexibility, and function.
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2

TAKIGUCHI, Yasuyuki, Ayako SHINA, and Tatsuaki YAMAGUCHI. "Bioconversion of D-glucosamine to D-glucosaminic acid." Journal of the agricultural chemical society of Japan 77, no. 6 (2003): 576–78. http://dx.doi.org/10.1271/nogeikagaku1924.77.576.

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3

&NA;. "Glucosamine." Reactions Weekly &NA;, no. 1167 (September 2007): 15. http://dx.doi.org/10.2165/00128415-200711670-00045.

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4

&NA;. "Glucosamine." Reactions Weekly &NA;, no. 1361 (July 2011): 23–24. http://dx.doi.org/10.2165/00128415-201113610-00081.

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5

&NA;. "Glucosamine." Reactions Weekly &NA;, no. 1205 (June 2008): 13. http://dx.doi.org/10.2165/00128415-200812050-00037.

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6

&NA;. "Glucosamine." Reactions Weekly &NA;, no. 1110 (July 2006): 10. http://dx.doi.org/10.2165/00128415-200611100-00030.

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7

Matheson, Anna J., and Caroline M. Perry. "Glucosamine." Drugs & Aging 20, no. 14 (2003): 1041–60. http://dx.doi.org/10.2165/00002512-200320140-00004.

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8

&NA;. "Glucosamine." Reactions Weekly &NA;, no. 1262 (July 2009): 14. http://dx.doi.org/10.2165/00128415-200912620-00043.

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9

&NA;. "Glucosamine." Reactions Weekly &NA;, no. 1033 (January 2005): 8. http://dx.doi.org/10.2165/00128415-200510330-00018.

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10

Barclay, Teresa Susanne, Candy Tsourounis, and Gary M. McCart. "Glucosamine." Annals of Pharmacotherapy 32, no. 5 (May 1998): 574–79. http://dx.doi.org/10.1345/aph.17235.

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OBJECTIVE: To review the pharmacology and pharmacokinetics of glucosamine and critically evaluate currently available literature regarding its safety and efficacy. DATA SOURCE: A MEDLINE search was conducted between January 1965 and May 1997. Key words used in the search were osteoarthritis, osteoarthrosis, gonarthrosis, and glucosamine. In addition, references cited in articles obtained from the MEDLINE search were reviewed for additional literature. STUDY SELECTION AND DATA EXTRACTION: All articles were considered for inclusion in the review. Articles were excluded from critical evaluation for lack of randomization, lack of a control group, 30 or fewer study participants, inconsistent treatment regimen, incomplete dosing information, or incomplete reporting of results. DATA SYNTHESIS: Osteoarthritis affects approximately 12% of the US population; the incidence increases with increasing age. Currently used pharmacologic treatments, including acetaminophen and nonsteroidal antiinflammatory drugs, do not slow or reverse the degenerative process in osteoarthritis. Glucosamine has recently received a great deal of attention from the public as a potential treatment of osteoarthritis, prompting healthcare professionals to investigate its clinical usefulness and potential for adverse effects. The drug has been proposed to stop and possibly reverse the degenerative process in osteoarthritis. Following absorption of an oral dose, glucosamine is incorporated into plasma proteins during first-pass metabolism, resulting in 26% bioavailability. Unbound glucosamine is concentrated in the articular cartilage. Each of the three critically evaluated studies reported a decrease in the symptoms of osteoarthritis (e.g., decreased Lequesne index, decreased pain severity, increased range of motion) for the glucosamine group, which was greater than that obtained in the control group. Flaws in study design, however, prevent the use of these results in modifying current clinical practice. Reported short-term adverse effects include mild gastrointestinal problems, drowsiness, skin reactions, and headache. CONCLUSIONS: Improvement in the symptoms of osteoarthritis associated with the use of glucosamine has been observed in clinical trials; however, those trials have flaws in design and data analysis. Further research needs to be conducted before glucosamine can be recommended as a treatment for osteoarthritis.
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11

BAUMANN, LESLIE S. "Glucosamine." Skin & Allergy News 40, no. 10 (October 2009): 14. http://dx.doi.org/10.1016/s0037-6337(09)70485-1.

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12

Meikle, P. J., A. M. Whittle, and J. J. Hopwood. "Human acetyl-coenzyme A:α-glucosaminide N-acetyltransferase. Kinetic characterization and mechanistic interpretation." Biochemical Journal 308, no. 1 (May 15, 1995): 327–33. http://dx.doi.org/10.1042/bj3080327.

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Acetyl-CoA: alpha-glucosaminide N-acetyltransferase (N-acetyltransferase) is an integral lysosomal membrane protein which catalyses the transfer of acetyl groups from acetyl-CoA on to the terminal glucosamine in heparin and heparan sulphate chains within the lysosome. In vitro, the enzyme is capable of acetylating a number of mono- and oligo-saccharides derived from heparin, provided that a non-reducing terminal glucosamine is present. We have prepared highly enriched lysosomal membrane fractions from human placenta by a combination of differential centrifugation and density-gradient centrifugation in Percoll. This preparation was used to investigate the kinetics of the enzyme with three acetyl-acceptor substrates, i.e. glucosamine and a disaccharide and a tetrasaccharide derived from heparin, each containing a terminal glucosamine residue. The enzyme showed a pH optimum at 6.5, extending to 8.0 for the mono- and di-saccharide substrates but falling off sharply above pH 6.5 for the tetrasaccharide substrate. We identified two distinct Km values for the glucosamine substrate at both pH 7.0 and pH 5.0, whereas the tetrasaccharide substrate displayed only a single Km value at each pH. The Km values were found to be highly pH-dependent, and at pH 5.0 the values for the acetyl-acceptor substrates showed a decreasing trend as the size of the substrate increased, suggesting that the enzyme recognizes an extended region of the non-reducing terminus of the heparin or heparan sulphate polysaccharides. Double-reciprocal analysis, isotope exchange between N-acetylglucosamine and glucosamine, and inhibition studies with desulpho-CoA indicate that the enzyme operates by a random-order ternary-complex mechanism. Product inhibition studies display a complex pattern of dead-end inhibition. Taken in context with what is known about lysosomal utilization and physiological levels of acetyl-CoA, these results suggest that in vivo the enzyme operates via a random-order ternary-complex mechanism which involves the utilization of cytosolic acetyl-CoA to transfer acetyl groups on to the terminal glucosamine residues of heparin within the lysosome.
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13

Pezzotti, Fabio, Hélène Therisod, and Michel Therisod. "Enzymatic synthesis of d-glucosaminic acid from d-glucosamine." Carbohydrate Research 340, no. 1 (January 2005): 139–41. http://dx.doi.org/10.1016/j.carres.2004.10.013.

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14

Kang, Hee Eun, Seung Jin Kim, Eun-ji Yeo, Jina Hong, Arun Rajgopal, Chun Hu, Mary A. Murray, Jennifer Dang, and Eunmi Park. "Pharmacokinetic Comparison of Chitosan-Derived and Biofermentation-Derived Glucosamine in Nutritional Supplement for Bone Health." Nutrients 14, no. 15 (August 5, 2022): 3213. http://dx.doi.org/10.3390/nu14153213.

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Glucosamine and chondroitin sulfate have been used as nutritional supplementation for joint tissues and osteoarthritis (OA). Biofermented glucosamine is of great interest in the supplement industry as an alternative source of glucosamine. The purpose of this study is to compare the pharmacokinetics of chitosan-derived glucosamine and biofermentation-derived glucosamine as nutritional supplementation. In a randomized, double-blind and cross-over study design, we recruited subjects of healthy men and women. The pharmacokinetics of glucosamine were examined after a single dose of glucosamine sulfate 2KCl (1500 mg) with two different sources of glucosamine (chitosan-derived glucosamine and biofermentation-derived glucosamine) to male and female subjects fitted with intravenous (iv) catheters for repeated blood sampling up to 8 h. According to plasma concentration–time curve of glucosamine after an oral administration of 1500 mg of glucosamine sulfate 2KCl, AUC0–8h and AUC0–∞ values of glucosamine following oral administration of chitosan-derived and biofermentation-derived glucosamine formulations were within the bioequivalence criteria (90% CI of ratios are within 0.8–1.25). The mean Cmax ratios for these two formulations (90% CI of 0.892–1.342) did not meet bioequivalence criteria due to high within-subject variability. There were no statistically significant effects of sequence, period, origin of glucosamine on pharmacokinetic parameters of glucosamine such as AUC0–8h, AUC0–∞, Cmax. Our findings suggest that biofermentation-derived glucosamine could be a sustainable source of raw materials for glucosamine supplement.
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15

KRAISANGSRI, Jittrakan, Sitthipong NALINANON, Siriporn RIEBROY, Suthasinee YARNPAKDEE, and Palanivel GANESAN. "Physicochemical Characteristics of Glucosamine from Blue Swimming Crab (Portunus pelagicus) Shell Prepared by Acid Hydrolysis." Walailak Journal of Science and Technology (WJST) 15, no. 12 (November 29, 2017): 869–77. http://dx.doi.org/10.48048/wjst.2018.3666.

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The aim of this research was to characterize glucosamine hydrochloride (GluHCl) from the shell of blue swimming crab (Portunus pelagicus). The crab shell was finely milled and processed to chitin prior to HCl hydrolysis using 30 % HCl for 30 min at 100 ºC for glucosamine production. The resultant glucosamine was recovered by crystallization using 95 % ethanol and was dried in a hot air oven. The color of the glucosamine crystals, expressed as L*, a*, and b*, was 83.01, 5.03, and -3.38, respectively. Crab shell glucosamine had high purity, which could be strongly stained by ninhydrin and presented at the same Rf of standard D-glucosamine using thin layer chromatography. Furthermore, prepared glucosamine exhibited similar Fourier transform infrared (FTIR) spectrum as standard D-glucosamine. Glucosamine from blue swimming crab shell had high purity as determined by HPLC and contained 808.15 mg D-glucosamine/g sample. The maximal transition temperature (Tmax) and the total enthalpy (ΔH) of prepared glucosamine were 194 ºC and 754.42 J/g, respectively. As a consequence, with the presented method, the resultant glucosamine was characterized to be D-glucosamine. Therefore, blue swimming crab shell, a byproduct from crab meat processing, has high potential as a raw material to produce glucosamine for food and nutraceutical applications.
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16

Leoni, S., A. D'Alessandro, R. Conti, M. Marino, S. Spagnuolo, and M. T. Mangiantini. "Seasonal pattern of glycosylation in frog liver." Bioscience Reports 11, no. 1 (February 1, 1991): 23–31. http://dx.doi.org/10.1007/bf01118602.

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The circannual behaviour of glycosylation and protein synthesis in frog liver slices was studied following the incorporation of3H-galactose and14C-glucosamine into glycolipids and glycoproteins and3H-leucine into proteins. The activity of two enzymes the galactosyl-transferase and the N-acetyl-glucosaminyl-1-P-transferase was determined. The incorporations of both sugars into the soluble fraction and into the lipid extract present a maximum during the spring-summer period. The incorporation into the protein fraction displays a different pattern:14C-Glucosamine and3H-leucine incorporation increases from winter to a maximum in autumn; the incorporation of3H-Galactose has a sharp peak during spring. The pattern of glycosyltransferase activities is similar to the pattern of incorporation of the two saccharides into proteins, indicating these enzymes as important control points for glycosylation in Anurae.
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17

McAlpine, Cameron S., Daniel R. Beriault, Tina Behdinan, Yuanyuan Shi, and Geoff H. Werstuck. "Oral glucosamine sulfate supplementation does not induce endoplasmic reticulum stress or activate the unfolded protein response in circulating leukocytes of human subjects." Canadian Journal of Physiology and Pharmacology 92, no. 4 (April 2014): 285–91. http://dx.doi.org/10.1139/cjpp-2013-0318.

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Glucosamine sulfate is a dietary supplement that is marketed as a treatment for osteoarthritis. Recent evidence from animal and cell culture models have suggested that glucosamine treatment can promote the misfolding of proteins and the activation of the unfolded protein response (UPR). We investigated whether glucosamine sulfate supplementation activates the UPR in circulating leukocytes of human subjects. Cultured Thp1 human monocytes were exposed to increasing concentrations of glucosamine (0, 0.25, 1.0, 4.0 mmol·L–1) for 18 h. We observed a dose-dependent increase in intracellular glucosamine levels as well as the activation of UPR. To test the effect of glucosamine sulfate supplementation in humans, 14 healthy human subjects took 1500 mg·day–1 glucosamine sulfate for 14 days. Metabolic parameters and blood samples were collected before and after supplementation. In humans, glucosamine sulfate supplementation did not alter metabolic parameters including lipid levels and glucose tolerance. Further, glucosamine sulfate supplementation did not affect intracellular glucosamine levels or activate the UPR in the leukocytes of human subjects. Our results indicate that in healthy human subjects, the recommended dose of glucosamine sulfate (1500 mg·day–1) for 14 days does not significantly alter intracellular glucosamine levels and does not activate the UPR in circulating leukocytes.
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18

Shultz, Suzanne M., and Esther Y. Dell. "Glucosamine/Chondroitin." Journal of Consumer Health On the Internet 10, no. 4 (October 17, 2006): 95–101. http://dx.doi.org/10.1300/j381v10n04_09.

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19

MCCOY, MICHAEL. "GLUCOSAMINE GAMBIT." Chemical & Engineering News Archive 81, no. 7 (February 17, 2003): 27–28. http://dx.doi.org/10.1021/cen-v081n007.p027.

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20

Pavelka, Karel. "32 GLUCOSAMINE." Osteoarthritis and Cartilage 14 (2006): S15—S16. http://dx.doi.org/10.1016/s1063-4584(07)60452-x.

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21

Reith, J., and C. Mayer. "Characterization of a Glucosamine/Glucosaminide N-Acetyltransferase of Clostridium acetobutylicum." Journal of Bacteriology 193, no. 19 (July 22, 2011): 5393–99. http://dx.doi.org/10.1128/jb.05519-11.

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22

Yu, Shengwu, Anika Singh, Huiying Zhang, and David D. Kitts. "An in vitro Method to Determine Intestinal Bioavailability of Glucosamine Salt Mixture." Journal of Nutritional Health & Food Science 9, no. 1 (February 10, 2021): 1–6. http://dx.doi.org/10.15226/jnhfs.2021.001180.

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Glucosamine is an amino sugar commonly used to improve joint health. It is often available for consumers as specialized supplements, the matrixes of which are formulated with components that facilitate enhancing functionality of the bioactive glucosamine. The primary objective of this study was to determine the in vitro bioaccessibility and bioavailability of a commercial glucosamine sulphate supplement, formulated with a mineral clay mixture. We used a modified a 3-step in vitro digestion procedure that included oral, gastric, and gastrointestinal digestions to assess bioaccessibility. Bioavailability followed using a Caco2 cell permeability test. Glucosamine bioaccessibility was not affected by gastric digestion and only marginally affected by gastrointestinal digestion (e.g., > 90% recovery). Bioavailability was dramatically lower, averaging approximately 15%, but similar for both the glucosamine reference standard and clay mineral mix glucosamine formulated product. Our in vitro bioavailability measurement of glucosamine, corrected for bioaccessibility, agree with values from in vitro rodent models. We conclude that the in vitro 3-step digestion of glucosamine, used to mimic gastrointestinal digestion, followed by the Caco2 permeability assay represents an alternative method to assess digestibility and bioavailability of formulated glucosamine products. Keywords: Glucosamine; Clay Mineral Mix; Bioaccessibility; Bioavailability
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23

Heart, Emma, Woo S. Choi, and Chin K. Sung. "Glucosamine-induced insulin resistance in 3T3-L1 adipocytes." American Journal of Physiology-Endocrinology and Metabolism 278, no. 1 (January 1, 2000): E103—E112. http://dx.doi.org/10.1152/ajpendo.2000.278.1.e103.

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To study molecular mechanisms for glucosamine-induced insulin resistance, we induced complete and reversible insulin resistance in 3T3-L1 adipocytes with glucosamine in a dose- and time-dependent manner (maximal effects at 50 mM glucosamine after 6 h). In these cells, glucosamine impaired insulin-stimulated GLUT-4 translocation. Glucosamine (6 h) did not affect insulin-stimulated tyrosine phosphorylation of the insulin receptor and insulin receptor substrate-1 and -2 and weakly, if at all, impaired insulin stimulation of phosphatidylinositol 3-kinase. Glucosamine, however, severely impaired insulin stimulation of Akt. Inhibition of insulin-stimulated glucose transport was correlated with that of Akt activity. In these cells, glucosamine also inhibited insulin stimulation of p70 S6 kinase. Glucosamine did not alter basal glucose transport and insulin stimulation of GLUT-1 translocation and mitogen-activated protein kinase. In summary, glucosamine induced complete and reversible insulin resistance in 3T3-L1 adipocytes. This insulin resistance was accompanied by impaired insulin stimulation of GLUT-4 translocation and Akt activity, without significant impairment of upstream molecules in insulin-signaling pathway.
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24

Elham Alshammari and Ahlam Alshammari. "Glucosamine effects on lipids and blood pressure." International Journal of Research in Pharmaceutical Sciences 11, no. 1 (January 9, 2020): 431–36. http://dx.doi.org/10.26452/ijrps.v11i1.1838.

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Glucosamine has in the past, been recommended for various functions, including the synthesis of synovial fluid, inhibiting degradation, and enhancing the healing of articular cartilage. However, there is no outstanding research that has been done to support these uses. The aim of the study is to examine the effects of glucosamine on lipids and blood pressure. Articles were obtained from reputable databases and used to discuss the glucosamine efficacy in osteoarthritis and glucosamine safety profile on lipids and blood pressure. The proposed study hypothesizes that glucosamine causes an increase in cholesterol and blood pressure levels. The authors analyzed past research studies on glucosamine, its efficacy in osteoarthritis, and the safety profile of the compound on lipids and blood pressure. The findings were inconclusive, even though they tended to suggest that glucosamine sulfate does not increase cholesterol levels; neither does it increase blood pressure in humans. Experimental research tended to show that glucosamine sulfate increases the levels of insulin, which might result in an increase in blood pressure. Even so, more recent studies have shown that glucosamine does not increase cholesterol levels; neither does the compound affect the blood pressure levels in human beings. Further studies are needed to ascertain the actual impact of glucosamine on lipids and blood pressure.
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25

Schelbach, Cheryl J., Rebecca L. Robker, Brenton D. Bennett, Ashley D. Gauld, Jeremy G. Thompson, and Karen L. Kind. "Altered pregnancy outcomes in mice following treatment with the hyperglycaemia mimetic, glucosamine, during the periconception period." Reproduction, Fertility and Development 25, no. 2 (2013): 405. http://dx.doi.org/10.1071/rd11313.

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Exposure of cumulus–oocyte complexes to the hyperglycaemia mimetic, glucosamine, during in vitro maturation impairs embryo development, potentially through upregulation of the hexosamine biosynthesis pathway. This study examined the effects of in vivo periconception glucosamine exposure on reproductive outcomes in young healthy mice, and further assessed the effects in overweight mice fed a high-fat diet. Eight-week-old mice received daily glucosamine injections (20 or 400 mg kg–1) for 3–6 days before and 1 day after mating (periconception). Outcomes were assessed at Day 18 of gestation. Glucosamine treatment reduced litter size independent of dose. A high-fat diet (21% fat) for 11 weeks before and during pregnancy reduced fetal size. No additional effects of periconception glucosamine (20 mg kg–1) on pregnancy outcomes were observed in fat-fed mice. In 16-week-old mice fed the control diet, glucosamine treatment reduced fetal weight and increased congenital abnormalities, but did not alter litter size. As differing effects of glucosamine were observed in 8-week-old and 16-week-old mice, maternal age effects were assessed. Periconception glucosamine at 8 weeks reduced litter size, whereas glucosamine at 16 weeks reduced fetal size. Thus, in vivo periconception glucosamine exposure perturbs reproductive outcomes in mice, with the nature of the outcomes dependent upon maternal age.
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26

Feng, Lijuan, Shanshan Zhang, Yan Zhou, Rongkai Pan, Hongchen Du, Fangfang Liu, and Yongqi Yang. "Expired Glucosamine Drugs as Green Corrosion Inhibitors for Carbon Steel in H2SO4 Solution and Synergistic Effect of Glucosamine Molecules with Iodide Ions: Combined Experimental and Theoretical Investigations." Crystals 13, no. 2 (January 23, 2023): 205. http://dx.doi.org/10.3390/cryst13020205.

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Glucosamine is a natural drug widely used for treating osteoarthritis and is usually left until it expires, which will cause a waste of resources if treated as garbage. However, its molecule contains many heteroatoms, entitling it to be a potential corrosion inhibitor. In this investigation, the corrosion inhibition activities of two types of expired glucosamine drugs (glucosamine hydrochloride and glucosamine sulfate) on carbon steel were estimated by electrochemical methods in the acidic solution. The results demonstrated that the glucosamine drugs were mixed-type corrosion inhibitors. Glucosamine hydrochloride could inhibit the carbon steel corrosion more significantly than that of sulfuric style at the same glucosamine content, suggesting a possible synergistic effect of glucosamine molecules with halide ions. Then, the co-adsorption behaviors of glucosamine sulfate with iodide ions were studied by experimental research, as well as theoretical investigations. The results indicated that the inhibition effect could be significantly enhanced when the glucosamine drug was utilized in combination with iodide ions. The electronic structures played a critical role in the synergistic inhibition of glucosamine drugs and iodide ions. Neutral molecules could interact with the metallic surface vertically through the amino and carbonyl groups, while protonated molecules were able to adsorb on it in parallel with the help of multiple functional groups. Since glucosamine molecules would be protonated and positively charged in the acidic solution, they were difficult to adsorb on the solid surface with metallic cations. When the iodide ions were presented, they preferentially adsorbed on the carbon steel surface and induced it to be negatively charged. Therefore, protonated glucosamine molecules could adsorb on the metallic surface using iodide ions as a bridge and form a protective film to mitigate the carbon steel corrosion.
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27

Nasution, Aurora Khairani. "Fabrication and Characterization of Glucosamine Hydrochloride from Chitin of Horseshoe Crab Shell (Tachypleus gigas)." Journal of Chemical Natural Resources 3, no. 2 (August 24, 2022): 147–54. http://dx.doi.org/10.32734/jcnar.v3i2.9350.

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Preparation of glucosamine hydrochloride from the chitin of horseshoe crab shells using the chemical hydrolysis method has been done using HCl concentration variation ratios of 7%, 9%, 11%,14 % with a ratio of 9:1 (v/w) for 4 hours at a temperature of 90ºC. Determination of glucosamine hydrochloride characteristics was characterized using Fourier transform-infra red (FT-IR) spectroscopy, in which the characteristics of glucosamine hydrochloride obtained in the OH group of glucosamine hydrochloride were 3446 cm-1 (s), 3448 cm-1 (s), 3450 cm-1 (s), 3448 cm-1 (s), respectively. For NH group of glucosamine hydrochloride were 1557 cm-1 (s), 1559 cm-1 (s), 1556 cm-1 (s), 1560 cm-1 (s), respectively. For CN group of glucosamine hydrochloride were 1379 cm-1 (m), 1379 cm-1 (m), 1379 cm-1 (m), 1379 cm-1 (m), respectively. While the glycoside bond of glucosamine hydrochloride 1073 cm-1 (w), 1074 cm-1 (w), 1074 cm-1 (w), 1074 cm-1 (w), respectively. Determination of the concentration of glucosamine hydrochloride with Ultraviolet Spectrophotometer analysis at a maximum wavelength of 197 nm with a standard solution of N-acetyl glucosamine in a solution of phosphate acid 0.005%, in which obtained the concentration of glucosamine hydrochloride 7% = 33.67 ppm, 9% = 36.35 ppm, 11% = 40.16 ppm, 14% = 43.97 ppm.
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28

WU, Guoyao, Tony E. HAYNES, Hui LI, Wene YAN, and Cynthia J. MEININGER. "Glutamine metabolism to glucosamine is necessary for glutamine inhibition of endothelial nitric oxide synthesis." Biochemical Journal 353, no. 2 (January 8, 2001): 245–52. http://dx.doi.org/10.1042/bj3530245.

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L-Glutamine is a physiological inhibitor of endothelial NO synthesis. The present study was conducted to test the hypothesis that metabolism of glutamine to glucosamine is necessary for glutamine inhibition of endothelial NO generation. Bovine venular endothelial cells were cultured for 24h in the presence of 0, 0.1, 0.5 or 2mM D-glucosamine, or of 0.2 or 2mM L-glutamine with or without 20µM 6-diazo-5-oxo-L-norleucine (DON) or with 100µM azaserine. Both DON and azaserine are inhibitors of L-glutamine:D-fructose-6-phosphate transaminase (isomerizing) (EC 2.6.1.16), the first and rate controlling enzyme in glucosamine synthesis. Glucosamine at 0.1, 0.5 and 2mM decreased NO production by 34, 45 and 56% respectively compared with controls where glucosamine was lacking. DON (20µM) and azaserine (100µM) blocked glucosamine synthesis and prevented the inhibition of NO generation by glutamine. Neither glutamine nor glucosamine had an effect on NO synthase (NOS) activity, arginine transport or cellular tetrahydrobiopterin and Ca2+ levels. However, both glutamine and glucosamine inhibited pentose cycle activity and decreased cellular NADPH concentrations; these effects of glutamine were abolished by DON or azaserine. Restoration of cellular NADPH levels by the addition of 1mM citrate also prevented the inhibiting effect of glutamine or glucosamine on NO synthesis. A further increase in cellular NADPH levels by the addition of 5mM citrate resulted in greater production of NO. Collectively, our results demonstrate that the metabolism of glutamine to glucosamine is necessary for the inhibition of endothelial NO generation by glutamine. Glucosamine reduces the cellular availability of NADPH (an essential cofactor for NOS) by inhibiting pentose cycle activity, and this may be a metabolic basis for the inhibition of endothelial NO synthesis by glucosamine.
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29

Abdul Kadir, Azidah, Arifah Abdul Kadir, Roslida Abd Hamid, Abdul Manan Mat Jais, Julia Omar, Abdul Nawfar Sadagatullah, Salziyan Badrin, Thin Thin Win, K. N. S. Sirajudeen, and Annas Salleh. "Evaluation of Chondroprotective Activity of Channa striatus in Rabbit Osteoarthritis Model." BioMed Research International 2019 (July 3, 2019): 1–11. http://dx.doi.org/10.1155/2019/6979585.

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Objectives. The objective of the study is to evaluate the chondroprotective activity of Channa striatus (Channa) and glucosamine sulphate (glucosamine) on histomorphometric examinations, serum biomarker, and inflammatory mediators in experimental osteoarthritis (OA) rabbit model. Design. Anterior cruciate ligament transection (ACLT) was performed to induce OA in thirty-three male New Zealand white rabbits and were randomly divided into three groups: Channa, glucosamine, and control group. The control group received drinking water and the Channa and glucosamine groups were orally administered with 51.4 mg/kg of Channa extract and 77.5 mg/kg of glucosamine sulphate in drinking water, respectively, for eight weeks and then sacrificed. The articular cartilage was evaluated macroscopically and histologically using semiquantitative and quantitative methods. Serum cartilage oligomeric matric protein (COMP), cyclooxygenase 2 (COX-2) enzyme, and prostaglandin E2 (PGE2) were also determined. Results. Macroscopic analysis revealed that Channa group have a significantly lower severity grade of total macroscopic score compared to the control (p < 0.001) and glucosamine (p < 0.05) groups. Semiquantitative histology scoring showed that both Channa and glucosamine groups had lower severity grading of total histology score compared to the control group (p < 0.001). In comparison with the control, Channa group had lower histopathological changes in three compartments of the joint compared to glucosamine group which had lower histological scoring in two compartments only. The cartilage thickness, area, and roughness of both Channa (p < 0.05) and glucosamine (p < 0.05) groups were superior compared to the control group. However, the Channa group demonstrated significantly less cartilage roughness compared to the glucosamine group (p < 0.05). Serum COMP levels were lower in both Channa (p < 0.05) and glucosamine (p < 0.05) groups compared to the control group. Conclusion. Both oral administration of Channa extract and glucosamine exhibited chondroprotective action on an ACLT OA-induced rabbit model. However, Channa was superior to glucosamine in maintaining the structure of the cartilage.
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Zhang, Pin, and Manote Sutheerawattananonda. "Kinetic Models for Glucosamine Production by Acid Hydrolysis of Chitin in Five Mushrooms." International Journal of Chemical Engineering 2020 (January 11, 2020): 1–8. http://dx.doi.org/10.1155/2020/5084036.

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In this paper, glucosamine was produced by acid hydrolysis of five mushrooms. The glucosamine yields were investigated, and the optimum conditions were obtained as follows: acid type, sulfuric acid; acid concentration, 6 M; ratio of raw material to acid volume, 1 : 10; hydrolysis temperature, 100°C; and time, 6 h. Under these conditions, the glucosamine conversion from chitin content reached up to 92%. The results of hydrolysis kinetics indicated that hydrolysis of five mushrooms to glucosamine followed zero-order kinetics. Moreover, the relatively low activation energy for hydrolysis of straw mushroom (18.31 kJ/mol) and the highest glucosamine yield (56.8132 ± 3.5748 mg/g DM, 0.9824 g/g chitin) indicated that hydrolysis of straw mushroom was energy-saving. Thus, sulfuric acid hydrolysis of straw mushroom for glucosamine production should be considered as an efficient process for the future industrial application. However, further study is needed for glucosamine purification.
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31

Schelbach, C., M. Lane, K. L. Kind, and J. G. Thompson. "235. Abberant murine embryonic development following glucosamine exposure during IVM or embryo culture." Reproduction, Fertility and Development 17, no. 9 (2005): 92. http://dx.doi.org/10.1071/srb05abs235.

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The hexosamine biosynthesis pathway is an alternate fate for glucose metabolism providing glycosylation moieties and is significantly upregulated by addition of glucosamine, a common dietary supplement. Here we determined the impact of glucosamine addition to cumulus oocyte complex (COC) maturation or during embryo culture on subsequent embryonic development. COCs were collected from 23-day-old mice 46 h post-eCG, and matured under several conditions prior to being fertilized and cultured: (1) 10mL/COC a MEM (5.56mM glucose) + 0, 1.25 or 5mM glucosamine; (2) 10mL/COC a MEM (20mM glucose) + 0, 1.25 or 5mM glucosamine; (3) 100mL/COC G2.3 (5mM glucose) + 0, 1.25 or 2.5mM glucosamine. One-cell embryos were also flushed from age-matched donors 24 h after mating and cultured in 0, 1.25 or 2.5mM glucosamine in G 1.3/2.3 sequential media. No differences in rates of embryonic development were detected between COCs matured in 10mL of media with 5.56mM glucose with glucosamine. However, blastocyst formation was significantly impaired (P<0.001) when COC maturation occurred in equivalent volumes of media that contained 20mM glucose + 1.25mM (49.98%) or 5mM glucosamine (44.7%) v. control (86.55%). Intriguingly, embryonic viability was significantly (P<0.001) reduced in COCs matured in 100mL G2.3 containing 5mM glucose + 1.25mM (44.6%) or 2.5mM glucosamine (40.1%) v. control (79.81%), suggesting a volume × glucose concentration interaction. In contrast, embryonic development was significantly reduced (34%, P < 0.002) and completely ablated when 1-cell embryos were cultured in media containing 1.25mM and 2.5mM glucosamine, respectively (control = 88.57%). These results suggest that glucosamine up-regulated hexosamine pathway activity in both COCs and early embryos impairs subsequent embryonic development by as yet undescribed mechanisms. Funded by NIH and NHMRC
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32

Le, Anh Quoc, Van Phu Dang, Ngoc Duy Nguyen, Quoc Hien Nguyen, and Dai Nghiep Ngo. "Preparation of chitosan-glucosamine derivatives (Maillard reaction products) by gamma Co-60 irradiation method and investigation of antibacterial activity." Nuclear Science and Technology 7, no. 2 (September 1, 2021): 44–50. http://dx.doi.org/10.53747/jnst.v7i2.111.

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The mixture solutions of glucosamine and chitosan with different molecular weights(123.5; 40.7 and 6.1 kDa) were irradiated by Co-60 gamma ray at dose of 50 kGy to prepare chitosanglucosamine Maillard reaction products (MRPs). The formation of MRPs was determined by measuring UV absorbance (at 284) nm and browning (at 420 nm). The reaction efficiency was calculated based on the ratio of reacted glucosamine and total added glucosamine. The antibacterial activity of chitosan-glucosamine MRPs against Escherichia coli was also investigated. The obtained results showed that the chitosan-glucosamine MRPs exhibited strong antibacterial activity, in which chitosan-glucosamine MRPs prepared from 123.5 kDa chitosan could reduce up to 4 log CFU/ml in comparison with the control (45 × 106 CFU/ml). Therefore, the chitosan-glucosamine MRPs prepared by the Co-60 gamma irradiation method can be potentially applied as a natural preservative for food, cosmetics and substituted for banned chemical preservatives.
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33

Bruyère, Olivier, Johann Detilleux, and Jean-Yves Reginster. "Health Technology Assessment of Different Glucosamine Formulations and Preparations Currently Marketed in Thailand." Medicines 10, no. 3 (March 8, 2023): 23. http://dx.doi.org/10.3390/medicines10030023.

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Objective: The aim of this study was to evaluate the cost-effectiveness of different glucosamine formulations and preparations used for the management of osteoarthritis in Thailand compared with placebo. Methods: We used a validated model to simulate the individual patient Utility score from aggregated data available from 10 different clinical trials. We then used the Utility score to calculate the quality-adjusted life year (QALY) over 3 and 6 months treatment period. We used the public costs of glucosamine products available in Thailand in 2019 to calculate the incremental cost-effectiveness ratio. We separated the analyses for prescription-grade crystalline glucosamine sulfate (pCGS) and other formulations of glucosamine. A cost-effectiveness cut-off of 3.260 USD/QALY was considered. Results: Irrespective of the glucosamine preparation (tablet or powder/capsule), the data show that pCGS is cost-effective compared with placebo over a 3 and 6 months. However, the other glucosamine formulations (e.g., glucosamine hydrochloride) never reached the breakeven point at any time. Conclusions: Our data show that pCGS is cost-effective for the management of osteoarthritis in the Thai context while other glucosamine formulations are not.
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34

Ciaraldi, Theodore P., Leslie Carter, Svetlana Nikoulina, Sunder Mudaliar, Donald A. McClain, and Robert R. Henry. "Glucosamine Regulation of Glucose Metabolism in Cultured Human Skeletal Muscle Cells: Divergent Effects on Glucose Transport/Phosphorylation and Glycogen Synthase in Non-Diabetic and Type 2 Diabetic Subjects1." Endocrinology 140, no. 9 (September 1, 1999): 3971–80. http://dx.doi.org/10.1210/endo.140.9.6974.

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Abstract Chronic exposure (48 h) to glucosamine resulted in a dose-dependent reduction of basal and insulin-stimulated glucose uptake activities in human skeletal muscle cell cultures from nondiabetic and type 2 diabetic subjects. Insulin responsiveness of uptake was also reduced. There was no change in total membrane expression of either GLUT1, GLUT3, or GLUT4 proteins. While glucosamine treatment had no significant effects on hexokinase activity measured in cell extracts, glucose phosphorylation in intact cells was impaired after treatment. Under conditions where glucose transport and phosphorylation were down regulated, the fractional velocity (FV) of glycogen synthase was increased by glucosamine treatment. Neither the total activity nor protein expression of glycogen synthase were influenced by glucosamine treatment. The stimulation of glycogen synthase by glucosamine was not due totally to soluble mediators. Reflective of the effects on transport/phosphorylation, total glycogen content and net glycogen synthesis were reduced after glucosamine treatment. These effects were similar in nondiabetic and type 2 cells. In summary: 1) Chronic treatment with glucosamine reduces glucose transport/phosphorylation and storage into glycogen in skeletal muscle cells in culture and impairs insulin responsiveness as well. 2) Down-regulation of glucose transport/phosphorylation occurs at a posttranslational level of GLUTs. 3) Glycogen synthase activity increases with glucosamine treatment. 4) Nondiabetic and type 2 muscle cells display equal sensitivity and responsiveness to glucosamine. Increased exposure of skeletal muscle to glucosamine, a substrate/precursor of the hexosamine pathway, alters intracellular glucose metabolism at multiple sites and can contribute to insulin resistance in this tissue.
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Wega Yusan Wira Perdana, Pirlina Umiastuti, Nabila Putri Wardhani, Amirah Jasmine, Nur Milati Bani Mostavan, Nadhilah Putri Ghaisani, and Audi Salman Faza. "THE USE OF GLUCOSAMINE AND THE INCREASE OF IOP: A LITERATURE REVIEW." Majalah Biomorfologi 32, no. 2 (July 9, 2022): 89–95. http://dx.doi.org/10.20473/mbiom.v32i2.2022.89-95.

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Highlights: 1. There are differences in the result of the use of glucosamine and the increase of intraocular pressure.2. There are many other factors that may contribute to the increase in the intraocular pressure other than the use of glucosamine such as races, genetics, different dose, and duration of glucosamine use. Abstract: Background: Glucosamine is an amino monosaccharide that can directly stimulate the synthesis of glycosaminoglycans in the cartilage. It has been widely used as an osteoarthritis treatment. However, several literatures show the possible side effects of glucosamine, such as increased intraocular pressure (IOP). Objective: The objective of this study was to determine if there was any correlation between the use of glucosamine and the increase in IOP. Material and Method: This was a descriptive qualitative study that implied a systematic review design. The study sample consisted of patients with osteoarthritis (OA) and glaucoma in Iran, Indonesia, Thailand, the USA, and India between 2013 and 2018. The literature search was conducted on a database (PubMed and Google Scholar) and selected using inclusion and exclusion criteria. Discussion: The research identified 5 studies on the use of glucosamine and the increase of IOP. Two articles provide significant results on the correlation between the use of glucosamine and the increase of IOP (P < 0.05). In addition, two studies showed significant IOP reduction outcomes after discontinuation of glucosamine (P < 0.05). A case series indicated an increase in IOP during the 6th month of glucosamine use but still at normal value. Conclusion: Many other factors contribute to IOP growth, other than the use of glucosamine. Therefore, a large-scale randomized clinical trial or a multicentre cohort study using the same parameters is still needed to improve the quality of the subsequent systematic review
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36

Martínez, Álvaro, Yanchao Lyu, Fabrizio Mancin, and Paolo Scrimin. "Glucosamine Phosphate Induces AuNPs Aggregation and Fusion into Easily Functionalizable Nanowires." Nanomaterials 9, no. 4 (April 17, 2019): 622. http://dx.doi.org/10.3390/nano9040622.

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The challenge to obtain plasmonic nanosystems absorbing light in the near infrared is always open because of the interest that such systems pose in applications such as nanotherapy or nanodiagnostics. Here we describe the synthesis in an aqueous solution devoid of any surfactant of Au-nanowires of controlled length and reasonably narrow dimensional distribution starting from Au-nanoparticles by taking advantage of the properties of glucosamine phosphate under aerobic conditions and substoichiometric nanoparticle passivation. Oxygen is required to enable the process where glucosamine phosphate is oxidized to glucosaminic acid phosphate and H2O2 is produced. The process leading to the nanosystems comprises nanoparticles growth, their aggregation into necklace-like aggregates, and final fusion into nanowires. The fusion requires the consumption of H2O2. The nanowires can be passivated with an organic thiol, lyophilized, and resuspended in water without losing their dimensional and optical properties. The position of the broad surface plasmon band of the nanowires can be tuned from 630 to >1350 nm.
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37

Le, Tuan, Thanh Hung Nguyen, Tuan Viet Nguyen, Thi Kieu Oanh Vu, Tuan Anh Pham, and Thanh Ha Le. "Evaluation of the growth of \(\textit{Vibrio natriegens}\) strains in a medium containing chitin derivatives and shrimp shell hydrolysate." Academia Journal of Biology 45, no. 4 (December 28, 2023): 73–82. http://dx.doi.org/10.15625/2615-9023/18777.

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Chitin from crustacean waste can be the future substrate for bioindustry towards the circular economy concept, especially for countries having large production of sea products like Vietnam. However, the chemical conversion of chitin into monomers implies high amounts of NaCl in a mixture with glucosamine, N-acetyl glucosamine, and acetate. Thus, a bacterial strain that can tolerate high salt concentration, and use chitin monomers as the sole carbon source such as Vibrio natriegens holds great potential in producing bioproducts from chitin derivatives. In this study, V. natriegens strains 10.3 and N5.3 isolated from Vietnam were compared with the reference strain V. natriegens DSM 759 for their growth performances in medium containing separately glucose and chitin monomers. Strain N5.3 showed the best growth rate among the 3 tested strains, exceptionally in medium containing glucosamine with nearly 1.5 times faster than strains 10.3 and DSM 759. Strain N5.3 cultured in bioreactor at 30 g/L NaCl indicated growth rate ranging from 0.614 to 0.881 h-1 in medium containing glucose, glucosamine, N-acetyl glucosamine, and shrimp shell hydrolysate. The formation of acetate was observed during the exponential growth of strain N5.3 in medium with glucose and N-acetyl glucosamine but not in medium with glucosamine or shrimp shell hydrolysate. The faster growth of all tested strains on N-acetyl glucosamine compared to glucosamine suggested metabolism of these substrates of V. natriegens similar to Eescherichia coli.
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38

Santosaningsih, Dewi, Yuanita Mulyastuti, Soeyati Poejiani, Rilia F. Putri, Liliana Dewi, Hisanifa Arifani, Yatim L. Ni’mah, and Afaf Baktir. "The Biofilm Inhibition Properties of Glucosamine Gold Nanoparticles in Combination with Meropenem against Pseudomonas aeruginosa on the Endotracheal Tube: A Model of Biofilm-Related Ventilator-Associated Pneumonia." Materials 17, no. 7 (March 31, 2024): 1604. http://dx.doi.org/10.3390/ma17071604.

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Biofilm-related infections play a significant role in the development and persistence of ventilator-associated pneumonia. Pseudomonas aeruginosa (P. aeruginosa) frequently causes biofilm-related infections associated with ventilator tubing. Glucosamine gold nanoparticles (AuNPs) may exhibit antibiofilm properties; however, more studies, including combinatorial therapy with antibiotics, are needed to explore their potential applications in clinical settings. This study aims to investigate the biofilm inhibition properties of glucosamine AuNPs in combination with meropenem against P. aeruginosa ATCC 9027 on the endotracheal tube. A biofilm inhibition assay of glucosamine AuNPs at 0.02 mg/mL, both singly and in combination with meropenem at 1 mg/mL, was carried out against P. aeruginosa ATCC 9027 on an endotracheal tube using the tissue culture plate method. Scanning electron microscopy was performed for visualization. Glucosamine AuNPs at 0.02 mg/mL combined with meropenem at 1 mg/mL showed greater biofilm inhibition (72%) on the endotracheal tube than glucosamine nanoparticles at 0.02 mg/mL alone (26%) (p = 0.001). The scanning electron microscopic visualization revealed that the untreated P. aeruginosa biofilm was denser than the glucosamine nanoparticles-treated biofilm, whether combined with meropenem or using glucosamine nanoparticles alone. The combination of glucosamine AuNPs and meropenem may have the synergistic effect of inhibiting biofilm production of P. aeruginosa on the endotracheal tubes of patients with mechanical ventilation. Conducting additional experiments to explore the impact of combining glucosamine-coated gold nanoparticles (AuNPs) with meropenem on the inhibition of biofilm production by clinical P. aeruginosa isolates would be beneficial.
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39

Kucharz, Eugene J., Volodymyr Kovalenko, Sándor Szántó, Olivier Bruyère, Cyrus Cooper, and Jean-Yves Reginster. "A review of glucosamine for knee osteoarthritis: why patented crystalline glucosamine sulfate should be differentiated from other glucosamines to maximize clinical outcomes." Current Medical Research and Opinion 32, no. 6 (February 26, 2016): 997–1004. http://dx.doi.org/10.1185/03007995.2016.1154521.

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40

McDowell, W., G. Weckbecker, D. O. R. Keppler, and R. T. Schwarz. "UDP-glucosamine as a substrate for dolichyl monophosphate glucosamine synthesis." Biochemical Journal 233, no. 3 (February 1, 1986): 749–54. http://dx.doi.org/10.1042/bj2330749.

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The sugar nucleotide analogue UDP-glucosamine was found to function as a sugar donor in microsomal preparations of both chick-embryo cells and rat liver, yielding dolichyl monophosphate glucosamine (Dol-P-GlcN). This was characterized by t.l.c. and retention by DEAE-cellulose. Glucosamine was the only water-soluble product released on mild acid hydrolysis. Dol-P-GlcN did not serve as substrate by transferring its glucosamine moiety to dolichol-linked oligosaccharide. Competition experiments between UDP-[3H]glucose and UDP-glucosamine showed Dol-P-[3H]glucose synthesis to be depressed by 56 or 73% in microsomes from chick-embryo cells and rat liver respectively. The concentrations of the UDP-sugars in this experiment were comparable with those occurring in galactosamine-metabolizing liver. These findings suggest that Dol-P-GlcN, formed as a metabolite of D-galactosamine, may interfere with Dol-P-dependent reactions.
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41

Sakai, K., and D. R. Clemmons. "Glucosamine Induces Resistance to Insulin-Like Growth Factor I (IGF-I) and Insulin in Hep G2 Cell Cultures: Biological Significance of IGF-I/Insulin Hybrid Receptors." Endocrinology 144, no. 6 (June 1, 2003): 2388–95. http://dx.doi.org/10.1210/en.2002-221133.

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Abstract IGF-I stimulates insulin-like actions directly through its receptor, and it also enhances sensitivity to insulin-mediated effects in vivo. These studies were undertaken to analyze the role of IGF-I, insulin, and insulin/IGF-I hybrid receptors (HRs) in mediating IGF-I and insulin signaling in cells that had been made insulin-resistant by treatment with glucosamine. Human HepG2 cells, which express IGF-I receptors, insulin receptors (IRs), and IGF-I/insulin HRs, were exposed to 20 mm glucosamine; and the effects of IGF-I and insulin in stimulating glycogen synthesis were determined. An overnight exposure to glucosamine markedly attenuated the effects of insulin and IGF-I in stimulating glycogen synthesis. To determine which receptors were mediating this effect, the ability of insulin and IGF-I to stimulate phosphorylation of their respective receptors was analyzed. An 18-h exposure to glucosamine (20 mm) caused a 75% reduction in the ability of IGF-I to phosphorylate its receptor but no change in receptor abundance. Glucosamine also caused a major reduction in insulin-stimulated receptor phosphorylation, although, unlike IGF-I, there was also a 50% reduction in IR abundance. Exposure to glucosamine also resulted in a reduction in the ability of IGF-I or insulin to stimulate phosphorylation of insulin IGF-I/HRs. The combination of insulin plus IGF-I was a more potent stimulus of HR phosphorylation than either agent alone, and this combination was also more potent in partially reversing the inhibitory effect of glucosamine. Taken together, these findings indicate that glucosamine induces a loss of sensitivity to stimulation of insulin, IGF-I, or HR tyrosine kinase activity by insulin or IGF-I. Although insulin is able to partially reverse the effect of glucosamine on IR phosphorylation, it has a very minimal effect on glucosamine-induced inhibition of HR phosphorylation. However, the combination of IGF-I and insulin induces a major increase in HR phosphorylation, even in the presence of glucosamine, suggesting that it is improving the sensitivity of the HR to insulin activation.
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42

McDowall, M. L. Sutton, R. B. Gilchrist, and J. G. Thompson. "204.Regulation of bovine oocyte meiotic and developmental capacity by glucose and glucosamine." Reproduction, Fertility and Development 16, no. 9 (2004): 204. http://dx.doi.org/10.1071/srb04abs204.

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Glucose is an important substrate for in vitro oocyte maturation (IVM) and is metabolised by cumulus oocyte complexes (COCs) via glycolysis or is used for extracellular matrix (ECM) synthesis. Follicular glucose concentration is significantly lower than commonly used IVM media (2.3�mM v. 5.6�mM in TCM199). Glucosamine is an alternative substrate for ECM and supplementation to IVM media reduces glucose uptake by COCs. The aim of this study was to determine the effect of glucose and glucosamine supplementation during IVM on bovine oocytes. First, bovine COCs (n�=�400) were matured in TCM199 (containing pyruvate, BSA, hCG and FSH), or synthetic follicular fluid medium (SFFM; a defined medium based on bovine follicular fluid composition) with 2.3�mM or 5.6�mM glucose���5�mM glucosamine and nuclear maturation was assessed after 24 and 30�h. Significantly less COCs matured in 2.3�mM glucose completed nuclear maturation compared to COCs matured in 5.6�mM glucose (P�<�0.05), whereas glucosamine had no effect on meiotic maturation. We then compared oocyte developmental capacity following IVM (n�=�600) in TCM199 or SFFM�+�5.6�mM glucose���5mM glucosamine. Blastocyst production was severely perturbed when COCs were matured in the presence of glucosamine (–glucosamine 32% v. +glucosamine 4%; P�<�0.001). To determine the cause of this reduction in oocyte developmental competence, we investigated oocyte protein synthesis by maturing COCs (n�=�100) in SFFM�+�5.6�mM glucose���5mM glucosamine�+�1�mM L-[2,3,4,5,6–3H] phenylalanine. In the presence of glucosamine, oocyte protein synthesis was reduced 40% compared to oocytes matured in control medium (P�<�0.05). These results demonstrate that while glucosamine supplementation has no effect on oocyte nuclear maturation, cytoplasmic maturation is compromised, as demonstrated by perturbed oocyte protein synthesis and embryo development. In contrast, glucose concentration has a significant influence on meiotic progression. This provides a useful model to investigate the mechanisms of establishment of developmental competence in oocytes following maturation.
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43

&NA;. "Glucosamine/hirsutine/probiotics." Reactions Weekly &NA;, no. 1263 (August 2009): 20. http://dx.doi.org/10.2165/00128415-200912630-00061.

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44

Blakeley, Judith A., and Violeta E. S. Ribeiro. "Glucosamine and Osteoarthritis." AJN, American Journal of Nursing 104, no. 2 (February 2004): 54–59. http://dx.doi.org/10.1097/00000446-200402000-00022.

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45

Cumming, Alistair. "Glucosamine in osteoarthritis." Lancet 354, no. 9190 (November 1999): 1640–41. http://dx.doi.org/10.1016/s0140-6736(05)77122-1.

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46

Russell, Alan I., and Mark F. McCarty. "Glucosamine in osteoarthritis." Lancet 354, no. 9190 (November 1999): 1641. http://dx.doi.org/10.1016/s0140-6736(05)77123-3.

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47

Adams, Mark. "Glucosamine in osteoarthritis." Lancet 354, no. 9190 (November 1999): 1641–42. http://dx.doi.org/10.1016/s0140-6736(05)77124-5.

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48

McCarty, M. F. "Glucosamine for psoriasis?" Medical Hypotheses 48, no. 5 (May 1997): 437–41. http://dx.doi.org/10.1016/s0306-9877(97)90043-8.

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49

Hume, Anne L. "Glucosamine and chondroitin." Pharmacy Today 25, no. 7 (July 2019): 16. http://dx.doi.org/10.1016/j.ptdy.2019.06.007.

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Adams, Mark E. "Hype about glucosamine." Lancet 354, no. 9176 (July 1999): 353–54. http://dx.doi.org/10.1016/s0140-6736(99)90040-5.

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