Glucosamina alert

[Eagle]

Lo sapete che la glucosamina (assunta per periodi di oltre pochi gg) provoca una netta insulino resistenza e negli esperimenti sugli animali viene usata per indurre il diabete?

E che sperimentalmente danneggia le cellule retiniche provocandone la morte prematura?


Eppure c'e' chi la considera una sostanza miracolosa, soprattutto per gli anziani con l'artrosi....una certa prudenza non farebbe mai male...si scoprono sempre novita'....perche' il "popolo del ferro" deve fare da cavia?


Eagle

[arabafenice]

Eagle mi passi lo studio o la documentazione che hai per questa notizia?

Grazie
A

[RAS]

speriamo ke non è vero.....

tra tutta l'insu ke mi sparo e la glucosamina ke prendo.........

[joepiada]

Re: Glucosamina alert

Originally posted by Eagle


E che sperimentalmente danneggia le cellule retiniche provocandone la morte prematura?

e io che pensavo di vederci male per via delle troppe pippe....

[Eagle]

Originally posted by arabafenice


Eagle mi passi lo studio o la documentazione che hai per questa notizia?

Grazie
A

Alcune cose, il resto lo devo cercare...

J Biol Chem 2002 Oct 18;277(42):39343-9

Immunosuppressive effects of glucosamine.

Ma L, Rudert WA, Harnaha J, Wright M, Machen J, Lakomy R, Qian S, Lu L, Robbins PD, Trucco M, Giannoukakis N.

Department of Surgery, T. E. Starzl Transplantation Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.

Glucosamine is a naturally occurring derivative of glucose and is an essential component of glycoproteins and proteoglycans, important constituents of many eukaryotic proteins. In cells, glucosamine is produced enzymatically by the amidation of glucose 6-phosphate and can then be further modified by acetylation to result in N-acetylglucosamine. Commercially, glucosamine is sold over-the-counter to relieve arthritis. Although there is evidence in favor of the beneficial effects of glucosamine, the mechanism is unknown. Our data demonstrate that glucosamine suppresses the activation of T-lymphoblasts and dendritic cells in vitro as well as allogeneic mixed leukocyte reactivity in a dose-dependent manner. There was no inherent cellular toxicity involved in the inhibition, and the activity was not reproducible with other amine sugars. More importantly, glucosamine administration prolonged allogeneic cardiac allograft survival in vivo. We conclude that, despite its documented effects on insulin sensitivity, glucosamine possesses immunosuppressive activity and could be beneficial as an immunosuppressive agent.



Metabolism 1998 May;47(5):573-7

Glucosamine infusion in rats mimics the beta-cell dysfunction of non-insulin-dependent diabetes mellitus.

Shankar RR, Zhu JS, Baron AD.

Department of Pediatrics, Indiana University School of Medicine, Indianapolis, USA.

Sustained hyperglycemia can cause peripheral insulin resistance and pancreatic beta-cell dysfunction and has been termed glucose toxicity or glucose-induced desensitization. Glucosamine, a product of glucose flux through the hexosamine biosynthetic pathway (HBP), causes insulin resistance in peripheral tissues and has been shown to cause abnormal glucose-insulin secretion coupling, and thus has been implicated in the pathogenesis of glucose toxicity. Here, we investigate whether glucosamine-induced insulin secretory dysfunction is specific to glucose or also extends to nonglucose secretagogues such as arginine. Two groups of 12 weight-matched Sprague-Dawley rats underwent hyperglycemic clamp studies (steady-state blood glucose, approximately 220 mg x dL(-1)) during infusion of normal saline or glucosamine 3.5 mg x kg(-1) x min(-1) over a 100-minute period. Insulin levels were measured at baseline and between 90 and 100 minutes. One hundred minutes into the hyperglycemic clamp, subgroups of seven rats each (saline- and glucosamine-infused rats) received a bolus of arginine (100 mg x kg(-1)) while the glucose infusion rate was unaltered. Glucose and insulin levels were measured at 1, 3, 5, 10, 15, and 30 minutes after the arginine bolus. Both groups had similar fasting glucose and insulin levels. At steady state (60 to 100 minutes), glucose levels were almost identical in both groups (223.58+/-3.94 v 224.58+/-4.34 mg x dL(-1)), but the glucose infusion rate (26.55+/-1.60 v 8.83+/-1.35 mg x kg(-1) x min(-1), P < .0001) and insulin level (41.36+/-6.47 v 18.04+/-2.95 mU x mL(-1), P < .0001) were markedly reduced in animals receiving glucosamine. Peak insulin levels 1 minute after the arginine bolus were lower in rats infused with glucosamine versus saline (274.00+/-30.38 v 176.25+/-20.12 microU x ml(-1), P=.0319). Total insulin secretion in response to arginine was significantly lower in the glucosamine group as determined by the area under the curve (1,268.09+/-142.27 v 706.77+/-84.79 microU x mL(-1) x min, P=.0054). In conclusion, glucosamine causes severe impairment in glucose-induced insulin secretion. Further, glucosamine-induced beta-cell secretory dysfunction extends to nonglycemic stimuli like arginine. This pattern of insulin secretory dysfunction is similar to that observed in patients with non-insulin-dependent diabetes mellitus (NIDDM). These data suggest that glucosamine may participate in the pathogenesis of glucose toxicity at the level of the beta cell in NIDDM patients.



Endocrinology 1999 Sep;140(9):3971-80

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 subjects.

Ciaraldi TP, Carter L, Nikoulina S, Mudaliar S, McClain DA, Henry RR.

Department of Medicine, University of California, San Diego, La Jolla 92093, USA.

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.
QUESTO E' FATTO SU ESSERI UMANI
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.




J Biol Chem 2001 Nov 23;276(47):43748-55

Excessive hexosamines block the neuroprotective effect of insulin and induce apoptosis in retinal neurons.

Nakamura M, Barber AJ, Antonetti DA, LaNoue KF, Robinson KA, Buse MG, Gardner TW.

Pennsylvania State Retina Research Group, The Ulerich Ophthalmology Research Center, the Department of Ophthalmology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA.

In addition to microvascular abnormalities, neuronal apoptosis occurs early in diabetic retinopathy, but the mechanism is unknown. Insulin may act as a neurotrophic factor in the retina via the phosphoinositide 3-kinase/Akt pathway. Excessive glucose flux through the hexosamine biosynthetic pathway (HBP) is implicated in the development of insulin resistance in peripheral tissues and diabetic complications such as nephropathy. We tested whether increased glucose flux through the HBP perturbs insulin action and induces apoptosis in retinal neuronal cells. Exposure of R28 cells, a model of retinal neurons, to 20 mm glucose for 24 h attenuated the ability of 10 nm insulin to rescue them from serum deprivation-induced apoptosis and to phosphorylate Akt compared with 5 mm glucose. Glucosamine not only impaired the neuroprotective effect of insulin but also induced apoptosis in R28 cells in a dose-dependent fashion. UDP-N-acetylhexosamines (UDP-HexNAc), end products of the HBP, were increased approximately 2- and 15-fold after a 24-h incubation in 20 mm glucose and 1.5 mm glucosamine, respectively. Azaserine, a glutamine:fructose-6-phosphate amidotransferase inhibitor, reversed the effect of 20 mm glucose, but not that of 1.5 mm glucosamine, on attenuation of the ability of insulin to promote cell survival and phosphorylate Akt as well as accumulation of UDP-HexNAc. Glucosamine also impaired insulin receptor processing in a dose-dependent manner but did not decrease ATP content. By contrast, in L6 muscle cells, glucosamine impaired insulin receptor processing but did not induce apoptosis. These results suggest that the excessive glucose flux through the HBP may direct retinal neurons to undergo apoptosis in a bimodal fashion; i.e. via perturbation of the neuroprotective effect of insulin mediated by Akt and via induction of apoptosis possibly by altered glycosylation of proteins. The HBP may be involved in retinal neurodegeneration in diabetes.

[sajan]

[sajan]

ho letto velocemnete gli articoli e di dosi mi pare non ne parlino o sbaglio??

[flexer77]

upi!

[ignifugo]

Re: Glucosamina alert

Originally posted by Eagle
Lo sapete che la glucosamina (assunta per periodi di oltre pochi gg) provoca una netta insulino resistenza e negli esperimenti sugli animali viene usata per indurre il diabete?

E che sperimentalmente danneggia le cellule retiniche provocandone la morte prematura?


Eppure c'e' chi la considera una sostanza miracolosa, soprattutto per gli anziani con l'artrosi....una certa prudenza non farebbe mai male...si scoprono sempre novita'....perche' il "popolo del ferro" deve fare da cavia?


Eagle

[Guru]

Essendo composta da glutammina e glucosio, era prevedibile un suo effetto sulla glicemia.
Anche i due sopra hanno gli stessi effetti, ma non drammatizzerei

Bye.

[NaturalMan]

Originally posted by Guru
Essendo composta da glutammina e glucosio, era prevedibile un suo effetto sulla glicemia.
Anche i due sopra hanno gli stessi effetti, ma non drammatizzerei

Bye.

daccordo ! inoltre ancora sono necessari ulterioristudi su essere umani in vivo non cells cultured .... cmq le sorprese possono essere sempre dietro l'angolo ...

Byeeeeeeeeeeeeeeeeeeeeeeeee