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MrMakaveli
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Anyone tried any other uncouplers aside from the two above or rather are there any worth trying?
Uncouplers besides DNP and UA
- Thread starter MrMakaveli
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drveejay11
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UA = Usnic Acid (Sodium Usinate)
GREAT question MAC.........BUMP!!!!!!
GREAT question MAC.........BUMP!!!!!!
variation
New member
Salicylic acid (aspirin)
though don't go overdosing on it now
and don't ask me for effective doses, I don't know these are side effects researchers noticed when studying the toxicity of it.
Indirect stimulation of respiration is caused by an increased production of CO2 as a result of salicylate-induced uncoupling of oxidative phosphorylation. Respiratory alkalosis develops as a result of the direct and indirect stimulation of the respiratory centre.
Oxidative Phosphorylation The uncoupling of oxidative phosphorylation by salicylate results in the inhibition of a number of ATP-dependent reactions and an increase in O2 uptake and CO2 production.
Nitrogen compound metabolism
Toxic doses of salicylate cause a significant nitrogen imbalance, characterized by amino aciduria, though this is due in part to stimulation of active tubular absorption because of reduced ATP formation.
Fat metabolism Salicylates enhance oxidation of fatty acids in muscle, liver and other tissues together with a decrease of concentrations of plasma, free fatty acids, phospholipids and cholesterol (Insel, 1996)
though don't go overdosing on it now
and don't ask me for effective doses, I don't know these are side effects researchers noticed when studying the toxicity of it.
Indirect stimulation of respiration is caused by an increased production of CO2 as a result of salicylate-induced uncoupling of oxidative phosphorylation. Respiratory alkalosis develops as a result of the direct and indirect stimulation of the respiratory centre.
Oxidative Phosphorylation The uncoupling of oxidative phosphorylation by salicylate results in the inhibition of a number of ATP-dependent reactions and an increase in O2 uptake and CO2 production.
Nitrogen compound metabolism
Toxic doses of salicylate cause a significant nitrogen imbalance, characterized by amino aciduria, though this is due in part to stimulation of active tubular absorption because of reduced ATP formation.
Fat metabolism Salicylates enhance oxidation of fatty acids in muscle, liver and other tissues together with a decrease of concentrations of plasma, free fatty acids, phospholipids and cholesterol (Insel, 1996)
MrMakaveli
New member
http://www.blackwell-synergy.com/links/doi/10.1046/j.1344-3941.2003.00144.x/enhancedabs/
Cashew Nut shell oil (AA) is apparently an uncoupler although finding AA seems very difficult.
There are others although the saftey of some is questionable.
Cashew Nut shell oil (AA) is apparently an uncoupler although finding AA seems very difficult.
There are others although the saftey of some is questionable.
drveejay11
New member
MrMakaveli said:
"An online subscription or single article purchase is required to access this article"macrophage69alpha
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aristolochic acid, the active component in cashew oil, is not an uncoupler, its a phospholipase A2 inhibitor. its is in the same class as arachidonic acid.
this is a supplement to be avoided
this is a supplement to be avoided
argent
New member
variation said:Salicylic acid (aspirin)
though don't go overdosing on it now
and don't ask me for effective doses, I don't know these are side effects researchers noticed when studying the toxicity of it.
Indirect stimulation of respiration is caused by an increased production of CO2 as a result of salicylate-induced uncoupling of oxidative phosphorylation. Respiratory alkalosis develops as a result of the direct and indirect stimulation of the respiratory centre.
Oxidative Phosphorylation The uncoupling of oxidative phosphorylation by salicylate results in the inhibition of a number of ATP-dependent reactions and an increase in O2 uptake and CO2 production.
Nitrogen compound metabolism
Toxic doses of salicylate cause a significant nitrogen imbalance, characterized by amino aciduria, though this is due in part to stimulation of active tubular absorption because of reduced ATP formation.
Fat metabolism Salicylates enhance oxidation of fatty acids in muscle, liver and other tissues together with a decrease of concentrations of plasma, free fatty acids, phospholipids and cholesterol (Insel, 1996)
can you post the study please?
MrMakaveli
New member
macrophage69alpha said:
Reducing effect of dietary anacardic acid on body fat pads in rats
Masaaki TOYOMIZU1, Katsuyuki OKAMOTO2, Teru ISHIBASHI2, Tetsuo NAKATSU3 and Yukio AKIBA1
ABSTRACT
We have previously shown that anacardic acid has an uncoupling effect on oxidative phosphorylation in rat liver mitochondria using succinate as a substrate (Toyomizu et al. 2000). In the present study, in order to clarify whether or not anacardic acid could be used advantageously as a special feed/food supplement to reduce fat deposition through the uncoupling action, two sets of experiments were conducted to determine quantitatively the effect of dietary anacardic acid (0.1% w/w) supplementation. More specifically, effects on growth, feed efficiency, fattening, and levels of several constituents of blood serum in rats fed normal and low protein-high carbohydrate (CHO) diets were examined. There were no significant differences in bodyweight gain, feed consumption and feed efficiency among the experimental groups. For the total fat pad content, including inguinal and epididymal fat, significant interaction was shown between both treatments: dietary anacardic acid at 0.1% w/w significantly decreased the total fat pad content in rats fed the CHO diet, but not in rats fed the normal diet. Weights of heart, spleen and brown adipose tissue were not affected by either the dietary treatment or anacardic acid, while both liver and kidney weights decreased with feeding of anacardic acid at 0.1% w/w, but were not affected by the CHO diet. Anacardic acid supplementation in the diet had no effect on serum glutamic oxaloacetic transaminase, alkaline phosphatase or lactate dehydrogenase levels, suggesting that the dysfunction of liver or kidney may not be induced by dietary anacardic acid. The results of the present study reveal a unique function of anacardic acid in that, for dietary conditions enhancing body fat deposition, that is consumption of a diet high in carbohydrates, dietary anacardic acid has the potential to decrease body fat deposition. A possible mechanism for differences observed in anacardic acid-induced regulation of body fat pad content between rats fed the normal and CHO diets, based on uncoupling action of anacardic acid on the mitochondrial oxidative phosphorylation, is discussed.
What about anacradic acid? (is what I'm talking about and what you mentioned the same thing?)
Any other uncuoplers worth an experiment Macro?
variation
New member
I believe it's based apon some research done in this study;
Lawson AAH, Proudfoot AT, Brown SS, et al.: Forced diuresis in
the treatment of acute salicylate poisoning in adults. Quart
J Med 38:31, 1969
can't get a copy of it online, if someone can, great.
here's some documentation on it;
http://www.intox.org/databank/documents/pharm/salicy/ukpid14.htm
though you did get me to work a little; and I did find this which helps us lay out some kind of quantitative figure in regards to comparison of salicylic acid and 2,4-dinitrophenol(dnp)
1: J Appl Physiol. 1982 Oct; 53(4): 925-9. Related Articles, Links
Effects of salicylate and 2,4-dinitrophenol on respiration and metabolism.
Millhorn DE, Eldridge FL, Waldrop TG.
The respiratory and metabolic responses to intravenous administration of sodium salicylate (240 mg/kg0.75) and 2,4-dinitrophenol (5.7 mg/kg0.75), uncouplers of oxidative phosphorylation, were studied in anesthetized, paralyzed, vagotomized, and glomectomized cats. During the initial 10 min after administration of salicylate, metabolic rate (VCO2) increased 70% and did not increase further during the experiment. Respiration, on the other hand, increased progressively at the same rate over the entire 60-min course of the experiment. The total increase in respiration was greater than 300%. Thus neither the time course nor the magnitude of the metabolic and respiratory responses were related. Similar findings were also obtained following administration of 2,4-dinitrophenol. We conclude that these agents stimulate respiration by a mechanism other than one related to the ability to uncouple oxidative phosphorylation and cause an increase in whole-body metabolism.
PMID: 6818204 [PubMed - indexed for MEDLINE]
btw, the MSDS reports that the mean lethal adult dose of salicylates is between 20 and 30 grams.
Lawson AAH, Proudfoot AT, Brown SS, et al.: Forced diuresis in
the treatment of acute salicylate poisoning in adults. Quart
J Med 38:31, 1969
can't get a copy of it online, if someone can, great.
here's some documentation on it;
http://www.intox.org/databank/documents/pharm/salicy/ukpid14.htm
though you did get me to work a little; and I did find this which helps us lay out some kind of quantitative figure in regards to comparison of salicylic acid and 2,4-dinitrophenol(dnp)
1: J Appl Physiol. 1982 Oct; 53(4): 925-9. Related Articles, Links
Effects of salicylate and 2,4-dinitrophenol on respiration and metabolism.
Millhorn DE, Eldridge FL, Waldrop TG.
The respiratory and metabolic responses to intravenous administration of sodium salicylate (240 mg/kg0.75) and 2,4-dinitrophenol (5.7 mg/kg0.75), uncouplers of oxidative phosphorylation, were studied in anesthetized, paralyzed, vagotomized, and glomectomized cats. During the initial 10 min after administration of salicylate, metabolic rate (VCO2) increased 70% and did not increase further during the experiment. Respiration, on the other hand, increased progressively at the same rate over the entire 60-min course of the experiment. The total increase in respiration was greater than 300%. Thus neither the time course nor the magnitude of the metabolic and respiratory responses were related. Similar findings were also obtained following administration of 2,4-dinitrophenol. We conclude that these agents stimulate respiration by a mechanism other than one related to the ability to uncouple oxidative phosphorylation and cause an increase in whole-body metabolism.
PMID: 6818204 [PubMed - indexed for MEDLINE]
btw, the MSDS reports that the mean lethal adult dose of salicylates is between 20 and 30 grams.
MrMakaveli
New member
variation said:
Interesting....
MrMakaveli
New member
Pyruvate and hydroxycitrate/carnitine may synergize to promote reverse electron transport in hepatocyte mitochondria, effectively 'uncoupling' the oxidation of fatty acids.
McCarty MF, Gustin JC.
NutriGuard Research, Encinitas, CA 92024, USA.
In a recent pilot study, joint administration of pyruvate, hydroxycitrate (HCA), and carnitine to obese subjects was associated with a remarkable rate of body-fat loss and thermogenesis, strongly suggestive of uncoupled fatty-acid oxidation. Hepatocytes possess an uncoupling mechanism--reverse electron transport--that enables fasting ketogenesis to proceed independent of respiratory control. Electrons entering the respiratory chain at the coenzyme Q (CoQ) level via FAD-dependent acyl coA dehydrogenase, can be driven 'up' the chain by the electrochemical proton gradient to reduce NAD+; if these electrons are then shuttled to the cytoplasm, returning to the respiratory chain at the CoQ level, the net result is heat generation at the expense of the proton gradient, enabling the uncoupled flow of electrons to oxygen. Pyruvate's bariatric utility may stem from its ability to catalyze the rapid transport of high-energy electrons from mitochondria to the cytoplasm, thus stimulating electron shuttle mechanisms. By enabling rapid mitochondrial uptake of fatty acids and thus disinhibiting hepatocyte ketogenesis, HCA/carnitine should initiate reverse electron transport: concurrent amplification of electron shuttle mechanisms by pyruvate can be expected to accelerate this reverse electron transport, thereby decreasing the electrochemical proton gradient. As a result, hepatocytes may be able to convert fatty acids to CO2 and heat with little net generation of ATP. These considerations suggest that it may be feasible to render hepatocytes functionally equivalent to activated brown fat, such that stored fat can be selectively oxidized in the absence of caloric restriction. Other measures which enhance the efficiency of hepatocyte electron shuttle mechanisms may increase the efficacy of this strategy.
I've heard this study is a little less than credible but the idea is interesting none the less.
McCarty MF, Gustin JC.
NutriGuard Research, Encinitas, CA 92024, USA.
In a recent pilot study, joint administration of pyruvate, hydroxycitrate (HCA), and carnitine to obese subjects was associated with a remarkable rate of body-fat loss and thermogenesis, strongly suggestive of uncoupled fatty-acid oxidation. Hepatocytes possess an uncoupling mechanism--reverse electron transport--that enables fasting ketogenesis to proceed independent of respiratory control. Electrons entering the respiratory chain at the coenzyme Q (CoQ) level via FAD-dependent acyl coA dehydrogenase, can be driven 'up' the chain by the electrochemical proton gradient to reduce NAD+; if these electrons are then shuttled to the cytoplasm, returning to the respiratory chain at the CoQ level, the net result is heat generation at the expense of the proton gradient, enabling the uncoupled flow of electrons to oxygen. Pyruvate's bariatric utility may stem from its ability to catalyze the rapid transport of high-energy electrons from mitochondria to the cytoplasm, thus stimulating electron shuttle mechanisms. By enabling rapid mitochondrial uptake of fatty acids and thus disinhibiting hepatocyte ketogenesis, HCA/carnitine should initiate reverse electron transport: concurrent amplification of electron shuttle mechanisms by pyruvate can be expected to accelerate this reverse electron transport, thereby decreasing the electrochemical proton gradient. As a result, hepatocytes may be able to convert fatty acids to CO2 and heat with little net generation of ATP. These considerations suggest that it may be feasible to render hepatocytes functionally equivalent to activated brown fat, such that stored fat can be selectively oxidized in the absence of caloric restriction. Other measures which enhance the efficiency of hepatocyte electron shuttle mechanisms may increase the efficacy of this strategy.
I've heard this study is a little less than credible but the idea is interesting none the less.
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Sigmund Roid
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The endogenous uncoupling protein UCP-2 is enhanced by T3 or T4.
Sigmund Roid
New member
This may be the reason why a lot of folks feel weak while on T3.
MrMakaveli
New member
Sigmund Roid said:
7-Keto apparently upregs UCP's as well
http://128.194.251.107/Ihler_home_page/7-oxo-DHEA.pdf
