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R-ala & S-ala
- Thread starter Diesel3d
- Start date
snakeman458
New member
you can get it at anabolicfitness.com
Diesel3d said:
I call this DECEITFUL What did you have to gain by not posting the ENTIRE section?!?! Yeah, I found the website, too.
CORRECT copy/paste:
Negative Results and Limitations
1. "For 6 wk, lean Zucker rats either remained sedentary, received R-ALA (30 mg. kg body wt(-1). day(-1)), performed exercise training (ET - treadmill running), or underwent both R-ALA treatment and ET. ET alone or in combination with R-ALA significantly increased (P < 0.05) peak oxygen consumption (28-31%) and maximum run time (52-63%). During an oral glucose tolerance test, ET alone or in combination with R-ALA resulted in a significant lowering of the glucose response (17-36%) at 15 min relative to R-ALA alone and of the insulin response (19-36%) at 15 min compared with sedentary controls. Insulin-mediated glucose transport activity was increased by ET alone in isolated epitrochlearis (30%) and soleus (50%) muscles, and this was associated with increased GLUT-4 protein levels. Insulin action was not improved by R-ALA alone, and ET-associated improvements in these variables were not further enhanced with combined ET and R-ALA. Although ET and R-ALA caused reductions in soleus protein carbonyls (an index of oxidative stress), these alterations were not significantly correlated with insulin-mediated soleus glucose transport. These results indicate that the beneficial interactive effects of ET and R-ALA on skeletal muscle insulin action observed previously in insulin-resistant obese Zucker rats are not apparent in insulin-sensitive lean Zucker rats."R
2. "we only observed a beneficial effect of [RLA] only in old and not in young animals."R
3. "The decline observed in the plasma concentration was steep (t1/2, 0.5 h)"R. ie RLA or RSLA have short plasma half-lives.
4. RLA did not improve "longer-term memory ... in the habituation in the open field test at a dose of 100 mg/kg body weight for 15 days ... for young mice"R.
You want the rest? The WHOLE story? Tune to:
http://morelife.org/supplements/RLA.html
-B
K
kronk
Guest
Isnt this study done on r+ala, and isnt the rala available r-ala? Just wondering and trying to figure this out.
That study is telling you that if you are a young lean rat r-ALA won't increase glucose uptake for you. Thankfully the members here are human and the results on human muscle cells show that r-ALA will increase glucose uptake dramatically.
Yaworsky K, Somwar R, Ramlal T, Tritschler HJ, Klip A. Engagement of the insulin-sensitive pathway in the stimulation of glucose transport by alpha-lipoic acid in 3T3-L1 adipocytes. Diabetologia. 2000 Mar;43(3):294-303.
Diabetes 1996 Dec;45(12):1798-804 Related Articles, Books, LinkOut
Stimulation of glucose uptake by the natural coenzyme alpha-lipoic acid/thioctic acid: participation of elements of the insulin signaling pathway.
Estrada DE, Ewart HS, Tsakiridis T, Volchuk A, Ramlal T, Tritschler H, Klip A.
Division of Cell Biology, Hospital for Sick Children, Toronto, Ontario, Canada.
Thioctic acid (alpha-lipoic acid), a natural cofactor in dehydrogenase complexes, is used in Germany in the treatment of symptoms of diabetic neuropathy. Thioctic acid improves insulin-responsive glucose utilization in rat muscle preparations and during insulin clamp studies performed in diabetic individuals. The aim of this study was to determine the direct effect of thioctic acid on glucose uptake and glucose transporters. In L6 muscle cells and 3T3-L1 adipocytes in culture, glucose uptake was rapidly increased by (R)-thioctic acid. The increment was higher than that elicited by the (S)-isomer or the racemic mixture and was comparable with that caused by insulin. In parallel to insulin action, the stimulation of glucose uptake by thioctic acid was abolished by wortmannin, an inhibitor of phosphatidylinositol 3-kinase, in both cell lines. Thioctic acid provoked an upward shift of the glucose-uptake insulin dose-response curve. The molar content of GLUT1 and GLUT4 transporters was measured in both cell lines. 3T3-L1 adipocytes were shown to have >10 times more glucose transporters but similar ratios of GLUT4:GLUT1 than L6 myotubes. The effect of (R)-thioctic acid on glucose transporters was studied in the L6 myotubes. Its stimulatory effect on glucose uptake was associated with an intracellular redistribution of GLUT1 and GLUT4 glucose transporters, similar to that caused by insulin, with minimal effects on GLUT3 transporters. In conclusion, thioctic acid stimulates basal glucose transport and has a positive effect on insulin-stimulated glucose uptake. The stimulatory effect is dependent on phosphatidylinositol 3-kinase activity and may be explained by a redistribution of glucose transporters. This is evidence that a physiologically relevant compound can stimulate glucose transport via the insulin signaling pathway.
Diabetologia 2000 Mar;43(3):294-303 Related Articles, Books, LinkOut
Engagement of the insulin-sensitive pathway in the stimulation of glucose transport by alpha-lipoic acid in 3T3-L1 adipocytes.
Yaworsky K, Somwar R, Ramlal T, Tritschler HJ, Klip A.
Hospital for Sick Children, Toronto, Ontario, Canada.
AIMS/HYPOTHESIS: A natural cofactor of mitochondrial dehydrogenase complexes and a potent antioxidant, alpha-lipoic acid improves glucose metabolism in people with Type II (non-insulin-dependent) diabetes mellitus and in animal models of diabetes. In this study we investigated the cellular mechanism of action of alpha-lipoic acid in 3T3-L1 adipocytes. METHODS: We treated 3T3-L1 adipocytes with 2.5 mmol/l R (+) alpha-lipoic acid for 2 to 60 min, followed by assays of: 2-deoxyglucose uptake; glucose transporter 1 and 4 (GLUT1 and GLUT4) subcellular localization; tyrosine phosphorylation of the insulin receptor or of the insulin receptor substrate-1 in cell lysates; association of phosphatidylinositol 3-kinase activity with immunoprecipitates of proteins containing phosphotyrosine or of insulin receptor substrate-1 using a in vitro kinase assay; association of the p85 subunit of phosphatidylinositol 3-kinase with phosphotyrosine proteins or with insulin receptor substrate-1; and in vitro activity of immunoprecipitated Akt1. The effect of R (+) alpha-lipoic acid was also compared with that of S(-) alpha-lipoic acid. RESULTS: Short-term treatment of 3T3-L1 adipocytes with R (+) alpha-lipoic acid rapidly stimulated glucose uptake in a wortmannin-sensitive manner, induced a redistribution of GLUT1 and GLUT4 to the plasma membrane, caused tyrosine phosphorylation of insulin receptor substrate-1 and of the insulin receptor, increased the antiphosphotyrosine-associated and insulin receptor substrate-1 associated phosphatidylinositol 3-kinase activity and stimulated Akt activity. CONCLUSION/INTERPRETATION: These results indicate that R (+) alpha-lipoic acid directly activates lipid, tyrosine and serine/threonine kinases in target cells, which could lead to the stimulation of glucose uptake induced by this natural cofactor. These properties are unique among all agents currently used to lower glycaemia in animals and humans with diabetes.
Yaworsky K, Somwar R, Ramlal T, Tritschler HJ, Klip A. Engagement of the insulin-sensitive pathway in the stimulation of glucose transport by alpha-lipoic acid in 3T3-L1 adipocytes. Diabetologia. 2000 Mar;43(3):294-303.
Diabetes 1996 Dec;45(12):1798-804 Related Articles, Books, LinkOut
Stimulation of glucose uptake by the natural coenzyme alpha-lipoic acid/thioctic acid: participation of elements of the insulin signaling pathway.
Estrada DE, Ewart HS, Tsakiridis T, Volchuk A, Ramlal T, Tritschler H, Klip A.
Division of Cell Biology, Hospital for Sick Children, Toronto, Ontario, Canada.
Thioctic acid (alpha-lipoic acid), a natural cofactor in dehydrogenase complexes, is used in Germany in the treatment of symptoms of diabetic neuropathy. Thioctic acid improves insulin-responsive glucose utilization in rat muscle preparations and during insulin clamp studies performed in diabetic individuals. The aim of this study was to determine the direct effect of thioctic acid on glucose uptake and glucose transporters. In L6 muscle cells and 3T3-L1 adipocytes in culture, glucose uptake was rapidly increased by (R)-thioctic acid. The increment was higher than that elicited by the (S)-isomer or the racemic mixture and was comparable with that caused by insulin. In parallel to insulin action, the stimulation of glucose uptake by thioctic acid was abolished by wortmannin, an inhibitor of phosphatidylinositol 3-kinase, in both cell lines. Thioctic acid provoked an upward shift of the glucose-uptake insulin dose-response curve. The molar content of GLUT1 and GLUT4 transporters was measured in both cell lines. 3T3-L1 adipocytes were shown to have >10 times more glucose transporters but similar ratios of GLUT4:GLUT1 than L6 myotubes. The effect of (R)-thioctic acid on glucose transporters was studied in the L6 myotubes. Its stimulatory effect on glucose uptake was associated with an intracellular redistribution of GLUT1 and GLUT4 glucose transporters, similar to that caused by insulin, with minimal effects on GLUT3 transporters. In conclusion, thioctic acid stimulates basal glucose transport and has a positive effect on insulin-stimulated glucose uptake. The stimulatory effect is dependent on phosphatidylinositol 3-kinase activity and may be explained by a redistribution of glucose transporters. This is evidence that a physiologically relevant compound can stimulate glucose transport via the insulin signaling pathway.
Diabetologia 2000 Mar;43(3):294-303 Related Articles, Books, LinkOut
Engagement of the insulin-sensitive pathway in the stimulation of glucose transport by alpha-lipoic acid in 3T3-L1 adipocytes.
Yaworsky K, Somwar R, Ramlal T, Tritschler HJ, Klip A.
Hospital for Sick Children, Toronto, Ontario, Canada.
AIMS/HYPOTHESIS: A natural cofactor of mitochondrial dehydrogenase complexes and a potent antioxidant, alpha-lipoic acid improves glucose metabolism in people with Type II (non-insulin-dependent) diabetes mellitus and in animal models of diabetes. In this study we investigated the cellular mechanism of action of alpha-lipoic acid in 3T3-L1 adipocytes. METHODS: We treated 3T3-L1 adipocytes with 2.5 mmol/l R (+) alpha-lipoic acid for 2 to 60 min, followed by assays of: 2-deoxyglucose uptake; glucose transporter 1 and 4 (GLUT1 and GLUT4) subcellular localization; tyrosine phosphorylation of the insulin receptor or of the insulin receptor substrate-1 in cell lysates; association of phosphatidylinositol 3-kinase activity with immunoprecipitates of proteins containing phosphotyrosine or of insulin receptor substrate-1 using a in vitro kinase assay; association of the p85 subunit of phosphatidylinositol 3-kinase with phosphotyrosine proteins or with insulin receptor substrate-1; and in vitro activity of immunoprecipitated Akt1. The effect of R (+) alpha-lipoic acid was also compared with that of S(-) alpha-lipoic acid. RESULTS: Short-term treatment of 3T3-L1 adipocytes with R (+) alpha-lipoic acid rapidly stimulated glucose uptake in a wortmannin-sensitive manner, induced a redistribution of GLUT1 and GLUT4 to the plasma membrane, caused tyrosine phosphorylation of insulin receptor substrate-1 and of the insulin receptor, increased the antiphosphotyrosine-associated and insulin receptor substrate-1 associated phosphatidylinositol 3-kinase activity and stimulated Akt activity. CONCLUSION/INTERPRETATION: These results indicate that R (+) alpha-lipoic acid directly activates lipid, tyrosine and serine/threonine kinases in target cells, which could lead to the stimulation of glucose uptake induced by this natural cofactor. These properties are unique among all agents currently used to lower glycaemia in animals and humans with diabetes.
ulter, why did you not post links to the source(s) of your information? It seems there's more to it. Again, I am not the advocate of either, or the detractor of either, but I want to know why people won't post links to their sources? That was my original objection in the first place.
When I read things like, "The effect of R (+) alpha-lipoic acid was also compared with that of S(-) alpha-lipoic acid. " and then the only piece addressed post-statement is R (+), then I have to wonder, did the person posting leave something out, or was this a very poorly written abstract? Either one calls suspicion to the validity of the information.
-B
When I read things like, "The effect of R (+) alpha-lipoic acid was also compared with that of S(-) alpha-lipoic acid. " and then the only piece addressed post-statement is R (+), then I have to wonder, did the person posting leave something out, or was this a very poorly written abstract? Either one calls suspicion to the validity of the information.
-B
young guns
New member
so what would be a recommended daily dose or r-ala. since it's been suggested that s-ala counteracts the effectiveness of the r enatiomer, then taking half as much r-ala still wouldn't be needed, correct? most people were seeing results at 2-3 grams of racemic mix of s and r, so would a single gram per day or r-ala be enough. even then, that could get costly, so what does everyone think the minimum amount to see results would be?
sorry if this was already answered and i missed it when reading the thread.
sorry if this was already answered and i missed it when reading the thread.
macrophage69alpha
New member
600mg of r-ala
