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Written by health and fitness sunday, 14 august 2005 glucosamine is readily produced in the human body & is necessary for the production of joint cartilage.
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Not only is it a building block for the synthesis of proteoglycans, its mere presence acts as a stimulus to the cells that produce proteoglycans – in fact glucosamine is a key factor in determining how many proteoglycans are produced by the cells.
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Glucosamine infusion into rats causes muscle insulin resistance without lowering P 37 ; , and, in the present study, that exposure of epitrochlearis muscles to glucosamine causes insulin resistance despite no decrease in ATP. We previously found 25 ; that prevention of an increase in UDP-HexNAc by inhibition of GFAT does not prevent glucose-induced insulin resistance and that inhibition of protein synthesis prevented glucoseinduced insulin resistance despite enhanced UDPHexNAc accumulation in skeletal muscle. This latter finding suggested the possibility that, like glucose, glucosamine might cause insulin resistance by inducing synthesis of a protein that mediates the insulin resistance. However, in contrast to the glucose-induced decrease in insulin responsiveness, the insulin resistance produced by exposing epitrochlearis muscles to glucosamine was not prevented by actinomycin D. As in previous studies on rats infused with glucosamine 28, 37 ; , exposure of epitrochlearis muscles to glucosamine resulted in a marked reduction of stimulation by insulin of IRS-1 tyrosine phosphorylation and IRS-1 association with PI3K. Under similar experimental conditions, glucose-induced insulin resistance was not associated with development of insulin resistance of these insulin-signaling events in epitrochlearis muscles 25 ; . It appears evident from these major differences that glucose and glucosamine induce skeletal muscle insulin resistance by different mechanisms. It has been proposed that glucosamine causes insulin resistance by impairing the functions of insulin-signaling proteins and GLUT4 by means of increased protein O-GlcNAcylation 3, 41 ; . Although it seems likely that this is the mechanism by which glucosamine causes insulin resistance, it is not clear whether this phenomenon has physiological relevance. The high concentrations of glucosamine required to produce muscle insulin resistance in animals infused with glucosamine and in muscles incubated with glucosamine in vitro are an experimental artifact, as glucosamine is normally too low to detect in plasma. In agreement with our finding that flooding of glucose into muscle can produce insulin resistance by a mechanism that does not involve hexosamine pathway end products 25, 26 ; , Robinson et al. 42 ; reported that an extreme degree of hyperglycemia resulted in insulin resistance despite only an 15% increase in UDP-HexNAcs. In conclusion, the results of this investigation and of previous studies 8, 28, 30, ; provide evidence that glucosamine and glucose induce insulin resistance by different mechanisms. In light of this evidence, and because exposure of tissues to glucosamine is unphysiological, it would appear that the appropriate approach to investigating the mechanisms underlying glucose toxicity is to flood muscle or adipose tissue with glucose, not glucosamine and glycopyrrolate.
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| Glucosamine sulphate 500mg14 another double-blind, placebo-controlled study evaluated chondroitin glucosamine for temporomandibular joint disease tmj ; but found equivocal results.
Amplified with HB-EGF primers set 1 ; from all endometrial RNA samples taken throughout the cycle. Set 2 HB-EGF primers also gave rise to a band at the predicted size 519 bp ; for HB-EGF cDNA data not shown ; . The amount of PCR product was similar from RNA taken at early and late proliferative, and early and late secretory stages of the cycle compare tracks 1-8 ; . Negative controls gave no product track 9 ; and positive cDNA controls gave a 340 bp band track 10 ; . Additional, non-specific bands were sometimes observed. The gel shown in the photograph in Figure 1 is representative of results obtained in many independent experiments. Efficient first strand synthesis was confirmed in each experiment by amplification of a 270 bp fibronectin cRNA from the same sample data not shown ; . Detection of HB-EGF mRNA in isolated stromal and epithelial cells is shown in Figure 2. HB-EGF was detected in both stroma tracks 1 and 2 ; and epithelium tracks 3 and 4 ; isolated from proliferative tracks 1 and 3 ; and secretory tracks 2 and 4 ; endometrium. HB-EGF is expressed in fetal and maternal placental tissues Detection of HB-EGF mRNA in first trimester decidua and chorionic villi, second trimester chorionic villi and term and goldenseal.
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KAREN MAGINNIS, ACCENTHEALTH HOST: JUST BECAUSE HERBAL SUPPLEMENTS HAVE BEEN LABELED NATURAL, IT DOESN'T NECESSARILY MEAN THEY'RE SAFE. DOCTORS WARN PATIENTS THAT BY MIXING HERBAL SUPPLEMENTS WITH MEDICATIONS, IT COULD DO MORE HARM THAN GOOD. CNN'S HOLLY FIRFER REPORTS ON ONE ELDERLY PATIENT'S EXPERIENCE. HOLLY FIRFER, ACCENTHEALTH REPORTER: ARLINE BRAGG IS CONSTANTLY BUSY WORKING AT HER RETIREMENT HOME, GOING TO CHURCH, AND MEETING FRIENDS. IT MAY BE HARD TO BELIEVE BUT THIS WOMAN IS 83-YEARS-OLD. SHE SAYS PEOPLE ASK HER ALL THE TIME HOW DOES SHE DO IT? ARLINE BRAGG: I have A, B, C, D, E, P, Calcium, Magnesium, Manganese, Zinc. I take Glucosamine and Chondroitin. FIRFER: ARLINE IS ONE OF OVER 60 MILLION AMERICANS WHO USE SOME SORT OF HERB OR VITAMIN PRODUCT. EXPERTS SAY THEY'VE SEEN A DRAMATIC INCREASE IN USE IN THE ELDERLY POPULATION. BUT THERE IS SOMETHING THESE PEOPLE NEED TO BE AWARE OF DOCTORS SAY MIXING SOME HERBS AND PRESCRIPTION DRUGS CAN CAUSE DANGEROUS REACTIONS. JOHN CARR, PHARMACIST: A lot of these herbs haven't been studied or put up against any drugs, or there's really no background on how they are going to react with things, and you could have problems you don't even know you're going to have. FIRFER: FOR INSTANCE, DRUGS USED TO TREAT HIGH BLOOD PRESSURE, DIABETES, AND HEART DISEASE ALL COMMON AILMENTS AS PEOPLE AGE SHOULD NOT BE TAKEN WITH PRODUCTS THAT CONTAIN EPHEDRA ALSO CALLED MA HUANG OR GINSENG, BOTH OF WHICH CAN INCREASE BLOOD PRESSURE. TAKING VITAMIN K, THE HERB FEVERFEW, OR GINKGO BILOBA WITH ANTI-CLOTTING DRUGS USED TO PREVENT STROKE LIKE COUMADIN OR PLAVIX CAN CAUSE HEMORRHAGING. DR. WILLIAM RICHARDSON, ATLANTA CLINIC OF PREVENTIVE MEDICINE: An elderly person using herbs unsupervised can be relatively dangerous. Even if you don't suffer from a medical problem do your research. CARR: A lot of the elderly look for a quick fix on things and sometimes they don't do quite the research, they just believe what they've heard on TV or what they've read in an advertisement. FIRFER: EXPERTS ADD, BE SURE TO TELL YOUR DOCTOR AND PHARMACIST ABOUT ANY HERBS AND VITAMINS YOU ARE TAKING BEFORE STARTING ANY NEW DRUG THERAPIES. HOLLY FIRFER, CNN, ATLANTA. MAGINNIS: THE ELDERLY ARE AMONG THE MILLIONS OF PEOPLE WHO ARE USING HERBS AND SUPPLEMENTS. BUT BEFORE YOU TRY AN ALTERNATIVE THERAPY, FIND OUT ALL YOU CAN AND ASK YOUR DOCTOR. YOU CAN ALSO VISIT THE ACCENTHEALTH WEBSITE AT accenthealth . OUR COMPLEMENTARY HEALTH CENTER HAS AN EASY-TO-USE DRUG INTERACTION GUIDE TO HELP YOU LEARN MORE ABOUT HERBS AND SUPPLEMENTS AND YOUR HEALTH.
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FIG. 1. Schematic representation of the experimental protocols used to assess the effects of increased glucosamine availability on the ability of insulin to activate PI3K in skeletal muscle. A, acute activation by bolus insulin: primed continuous infusions of GlcN 750 mmol kg bolus; 30 mmol kg min ; or saline were maintained for 2 h in fasted, conscious, and nondiabetic rats. 1 unit kg intravenous insulin bolus was administered 2 min prior to sacrifice. B, 3-h euglycemic, hyperinsulinemic clamp studies: primed continuous infusions of GlcN 750 mmol kg bolus; 30 mmol kg min ; were maintained throughout 3-h euglycemic, hyperinsulinemic 18 milliunits kg min; 500 microunits ml ; clamps in conscious, nondiabetic rats n 5 ; , while 3-h time control insulin clamp studies were performed in an additional n 6 saline-infused rats. Euglycemia 130 mg dl ; was maintained with variable infusion rates of a 25% glucose solution. Infusions of [3-3H]glucose were used to measure rates of peripheral glucose uptake and glycolysis. C, time course studies: euglycemic, hyperinsulinemic 18 milliunits kg min ; clamps were performed for 2 h in conscious, nondiabetic rats with infusion of [3-3H3]glucose to measure rates of peripheral glucose uptake. GlcN 750 mmol kg bolus; 30 mmol kg min ; was infused during the final 30 min 30 , n 5 ; , min 60 , n 5 ; , min 90 , n 5 ; throughout 120 , n 5 ; the 2-h studies. Time control euglycemic, hyperinsulinemic 18 milliunits kg min ; clamp studies were performed with infusion of saline for 2 h in additional n 12 rats. were obtained for determination of [3H]glucose-specific activity, insulin, and GlcN concentrations as described above. Basal Studies--Assessment of basal PI3K activity was performed in additional fasting animals in the presence of 2-h infusions of GlcN 750 mol kg bolus, then 30 mol kg min; n 8 ; or saline n 12 and granisetron.
Phate may act in the same fashion as glucose B-phosphate but to a lesser degree. It also appears that the presence of inorganic phosphate partially inhibits glucose B-phosphate activation. At pH 7.2, in a l.O-ml incubation mixture containing 10 mM glucose A-phosphate, 10 mM fructose B-phosphate, and 20 ells NH&I, the specific activity is 45 nmoles of glucosamine 6-phosphate per min per mg of protein if buffered by 50 pmoles of Tris-HCI, but only 34 nmoles of glucosamine 6-phosphate per.
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3. Sanders JE, Thomas ED, Buckner, CD. et al. Marrow transplantation for children in first remission of acute non-lymphoblastic leukemia: an update. Blood 1985; 66: 460-462.
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