TheCrownedOne
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After I saw bulk pyruvate (kilo for $28) at proteincustomizer I figured I'd find a couple pubmed studies. These are just a couple I snagged for your personal perusal:
Pyruvate and hydroxycitrate/carnitine may synergize to promote reverse electron transport in hepatocyte mitochondria, effectively 'uncoupling' the oxidation of fatty acids.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10416948
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.
Publication Types:
Review
Review, Tutorial
PMID: 10416948 [PubMed - indexed for MEDLINE]
Effect of pyruvate and dihydroxyacetone on metabolism and aerobic endurance capacity.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9624640
Ivy JL.
Department of Kinesiology and Health Education, University of Texas at Austin, USA. [email protected]
Pyruvate and dihydroxyacetone are three carbon compounds that when infused directly into the blood or taken orally produce strong metabolic effects. When chronically fed to animals as part of their diet, pyruvate plus dihydroxyacetone reduce the rate of weight gain and body fat content during growth. These alterations in growth pattern appear to be the result of an increased loss of calories as heat at the expense of storage of lipid. Pyruvate-dihydroxyacetone supplementation has also been found to improve the insulin sensitivity of insulin resistant rats and reduce plasma cholesterol levels induced by a high cholesterol diet as well as lower blood pressure and heart rate in obese individuals. When infused in rats during prolonged treadmill running, pyruvate reduced run time to exhaustion by approximately 67%. However, when provided as an oral supplement for several days, it has enhanced aerobic endurance capacity. The mechanism of action is unclear, but available data suggest that the increase in performance following pyruvate-dihydroxyacetone supplementation may be a result of an increased reliance on blood glucose, thus sparing muscle glycogen. In summary, chronic supplementation of pyruvate-dihydroxyacetone may be beneficial from a preventive medicine prospective as well as for certain athletic endeavors.
Publication Types:
Review
Review, Tutorial
PMID: 9624640 [PubMed - indexed for MEDLINE]
Inhibition of regain in body weight and fat with addition of 3-carbon compounds to the diet with hyperenergetic refeeding after weight reduction.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8910097
Stanko RT, Arch JE.
Department of Medicine, Montefiore University Hospital, University of Pittsburgh Medical Center, PA 15213-2582, USA.
OBJECTIVE: To investigate the efficacy of the 3-carbon compounds pyruvate and dihydroxyacetone (PD) in inhibiting reaccumulation of body weight and fat with refeeding after weight loss. DESIGN: Longitudinal, in Clinical Research Center. After weight loss induced by hypoenergetic diet (1.3 MJ/d) for 3 weeks, refeeding with hyperenergetic diet (1.5 x resting energy expenditure) for 3 weeks. Refeeding diet randomized to contain PD or placebo (PL, polyglucose) as approximately 20% of energy intake. SUBJECTS: 17 obese healthy women (n = 8 in PL group, n = 9 in PD group) (age: 22-60 y, weight: 72.5-139.7 kg). MEASUREMENTS: Resting energy expenditure (REE), body composition (by bioelectrical impedance), nitrogen balance, serum proteins, biochemical profile, thyroid hormones, and insulin, before and after refeeding and weight and fat gain. RESULTS: Refeeding with a hyperenergetic diet, weight gain was significantly less in patients receiving PD compared to placebo (1.8 + 0.2 kg vs 2.9 +/- 0.1 kg, P < 0.01). Body fat regain was also less with feeding of PD (0.8 +/- 0.2 kg vs 1.8 +/- 0.2 kg, P < 0.01). Body protein metabolism, as measured by nitrogen balance, serum protein concentrations and fat free mass, was similar in subjects consuming either PD or PL. CONCLUSIONS: We conclude that 3-carbon compounds decrease weight gain and reaccumulation of body fat, without decreasing body protein gain, in obese subjects with hyperenergetic refeeding subsequent to weight loss.
Publication Types:
Clinical Trial
Randomized Controlled Trial
PMID: 8910097 [PubMed - indexed for MEDLINE]
The good news on green tea will never end I'm afraid:
Green tea extract (AR25(R)) inhibits lipolysis of triglycerides in gastric and duodenal medium in vitro.
Juhel C, Armand M, Pafumi Y, Rosier C, Vandermander J, Lairon D.
Unit 476-INSERM,zcasex> (Institut National de la Sante et de la Recherche Medicale), Marseille, France.
In this study, we aimed to evaluate in vitro the inhibitory activity of a green tea extract (AR25(R) standardized at 25% catechins) on gastric and pancreatic lipase activities. We first used tributyrin as a substrate to evaluate the capability of AR25 to induce digestive lipase inhibition. Gastric lipase was totally inhibited by 40 mg AR25/g tributyrin whereas pancreatic lipase inhibition was maximum (78.8 +/- 0.7%) with 80 mg AR25/g tributyrin. We then used triolein, a long-chain triglyceride, to check whether AR25 could alter lipase activities on a physiologic substrate. AR25 60 mg/g triolein induced a dramatic inhibition of gastric lipase (96.8 +/- 0.4%) whereas pancreatic lipase activity was partially reduced (66.50 +/- 0.92%). Finally, the concerted action of gastric and pancreatic lipases was studied with an excess of enzymes to mimic the physiologic conditions observed in vivo. Incubation of AR25 with an excess of digestive lipases resulted in a drastic decrease in gastric lipolysis but the inhibitory effect on pancreatic lipase was less marked. On the whole, as compared to the control, lipolysis of triolein under the successive action of the two digestive lipases was reduced by 37 +/- 0.6% in the presence of AR25. Because a lipid/water interface is necessary for lipolysis to occur, lipid emulsification and emulsion droplet size were measured in gastric and duodenal media in the presence of AR25. In gastric and duodenal conditions, AR25 inhibited the lipid emulsification process. From these data we conclude that (1) in vitro, fat digestion is significantly inhibited by 60 mg AR25/g triolein, and (2) gastric as well as pancreatic lipase inhibition could be related to altered lipid emulsification in gastric or duodenal media. The green tea extract AR25 exhibiting marked inhibition of digestive lipases in vitro is likely to reduce fat digestion in humans.
PMID: 15539342 [PubMed - in process]
The green tea polyphenol (-)-epigallocatechin gallate and green tea can protect human cellular DNA from ultraviolet and visible radiation-induced damage.
Morley N, Clifford T, Salter L, Campbell S, Gould D, Curnow A.
Cornwall Dermatology Research Project, Polgooth Ward, Royal Cornwall Hospital, Treliske, Truro, Cornwall, UK.
Background: Antioxidant compounds in green tea may be able to protect against skin carcinogenesis and it is of interest to investigate the mechanisms involved. A study was therefore conducted to determine whether the isolated green tea polyphenol (-)-epigallocatechin gallate (EGCG) could prevent ultraviolet radiation (UVR)-induced DNA damage in cultured human cells. This work was then extended to investigate whether drinking green tea could afford any UVR protection to human peripheral blood cells collected after tea ingestion. Methods: The alkaline comet assay was used to compare the DNA damage induced by UVR in cultured human cells with and without the presence of EGCG. The same assay technique was then employed to assess UVR-induced DNA damage in peripheral leucocytes isolated from 10 adult human volunteers before and after drinking 540 ml of green tea. Results: Initial trials found that EGCG afforded concentration-dependent photoprotection to cultured human cells with a maximal activity at a culture concentration of 250 muM. The cells types tested (lung fibroblasts, skin fibroblasts and epidermal keratinocytes) demonstrated varying susceptibility to the UVR insult provided. The in vivo trials of green tea also demonstrated a photoprotective effect, with samples of peripheral blood cells taken after green tea consumption showing lower levels of DNA damage than those taken prior to ingestion when exposed to 12 min ultraviolet A (UVA) radiation. Conclusion: The studies showed that green tea and/or some constituents can offer some protection against UV-induced DNA damage in human cell cultures and also in human peripheral blood samples taken post-tea ingestion.
PMID: 15634219 [PubMed - in process]
Anti-obesity actions of green tea: Possible involvements in modulation of the glucose uptake system and suppression of the adipogenesis-related transcription factors.
Ashida H, Furuyashiki T, Nagayasu H, Bessho H, Sakakibara H, Hashimoto T, Kanazawa K.
Department of Biofunctional Chemistry, Faculty of Agriculture, Kobe University, Rokkodai, Nada-ku, Kobe 657-8501, Japan.
To investigate mechanisms of the anti-obesity actions of green tea in vivo, rats were given green tea instead of drinking water for 3 weeks. It was confirmed that green tea reduced adipose tissue weight without any change in body weight, other tissue weights, and food and water intakes. Green tea also significantly reduced the plasma levels of cholesterols and free fatty acids. Certain catechins existed in the plasma at 0.24 microM under our experimental conditions, though most of them existed as conjugated forms. For mechanisms of the anti-obesity actions, green tea significantly reduced glucose uptake accompanied by a decrease in translocation of glucose transporter 4 (GLUT4) in adipose tissue, while it significantly stimulated the glucose uptake with GLUT4 translocation in skeletal muscle. Moreover, green tea suppressed the expression of peroxisome proliferator-activated receptor gamma and the activation of sterol regulatory element binding protein-1 in adipose tissue. In conclusion, green tea modulates the glucose uptake system in adipose tissue and skeletal muscle and suppresses the expression and/or activation of adipogenesis-related transcription factors, as the possible mechanisms of its anti-obesity actions.
PMID: 15630268 [PubMed - in process]
Pyruvate and hydroxycitrate/carnitine may synergize to promote reverse electron transport in hepatocyte mitochondria, effectively 'uncoupling' the oxidation of fatty acids.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10416948
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.
Publication Types:
Review
Review, Tutorial
PMID: 10416948 [PubMed - indexed for MEDLINE]
Effect of pyruvate and dihydroxyacetone on metabolism and aerobic endurance capacity.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9624640
Ivy JL.
Department of Kinesiology and Health Education, University of Texas at Austin, USA. [email protected]
Pyruvate and dihydroxyacetone are three carbon compounds that when infused directly into the blood or taken orally produce strong metabolic effects. When chronically fed to animals as part of their diet, pyruvate plus dihydroxyacetone reduce the rate of weight gain and body fat content during growth. These alterations in growth pattern appear to be the result of an increased loss of calories as heat at the expense of storage of lipid. Pyruvate-dihydroxyacetone supplementation has also been found to improve the insulin sensitivity of insulin resistant rats and reduce plasma cholesterol levels induced by a high cholesterol diet as well as lower blood pressure and heart rate in obese individuals. When infused in rats during prolonged treadmill running, pyruvate reduced run time to exhaustion by approximately 67%. However, when provided as an oral supplement for several days, it has enhanced aerobic endurance capacity. The mechanism of action is unclear, but available data suggest that the increase in performance following pyruvate-dihydroxyacetone supplementation may be a result of an increased reliance on blood glucose, thus sparing muscle glycogen. In summary, chronic supplementation of pyruvate-dihydroxyacetone may be beneficial from a preventive medicine prospective as well as for certain athletic endeavors.
Publication Types:
Review
Review, Tutorial
PMID: 9624640 [PubMed - indexed for MEDLINE]
Inhibition of regain in body weight and fat with addition of 3-carbon compounds to the diet with hyperenergetic refeeding after weight reduction.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8910097
Stanko RT, Arch JE.
Department of Medicine, Montefiore University Hospital, University of Pittsburgh Medical Center, PA 15213-2582, USA.
OBJECTIVE: To investigate the efficacy of the 3-carbon compounds pyruvate and dihydroxyacetone (PD) in inhibiting reaccumulation of body weight and fat with refeeding after weight loss. DESIGN: Longitudinal, in Clinical Research Center. After weight loss induced by hypoenergetic diet (1.3 MJ/d) for 3 weeks, refeeding with hyperenergetic diet (1.5 x resting energy expenditure) for 3 weeks. Refeeding diet randomized to contain PD or placebo (PL, polyglucose) as approximately 20% of energy intake. SUBJECTS: 17 obese healthy women (n = 8 in PL group, n = 9 in PD group) (age: 22-60 y, weight: 72.5-139.7 kg). MEASUREMENTS: Resting energy expenditure (REE), body composition (by bioelectrical impedance), nitrogen balance, serum proteins, biochemical profile, thyroid hormones, and insulin, before and after refeeding and weight and fat gain. RESULTS: Refeeding with a hyperenergetic diet, weight gain was significantly less in patients receiving PD compared to placebo (1.8 + 0.2 kg vs 2.9 +/- 0.1 kg, P < 0.01). Body fat regain was also less with feeding of PD (0.8 +/- 0.2 kg vs 1.8 +/- 0.2 kg, P < 0.01). Body protein metabolism, as measured by nitrogen balance, serum protein concentrations and fat free mass, was similar in subjects consuming either PD or PL. CONCLUSIONS: We conclude that 3-carbon compounds decrease weight gain and reaccumulation of body fat, without decreasing body protein gain, in obese subjects with hyperenergetic refeeding subsequent to weight loss.
Publication Types:
Clinical Trial
Randomized Controlled Trial
PMID: 8910097 [PubMed - indexed for MEDLINE]
The good news on green tea will never end I'm afraid:
Green tea extract (AR25(R)) inhibits lipolysis of triglycerides in gastric and duodenal medium in vitro.
Juhel C, Armand M, Pafumi Y, Rosier C, Vandermander J, Lairon D.
Unit 476-INSERM,zcasex> (Institut National de la Sante et de la Recherche Medicale), Marseille, France.
In this study, we aimed to evaluate in vitro the inhibitory activity of a green tea extract (AR25(R) standardized at 25% catechins) on gastric and pancreatic lipase activities. We first used tributyrin as a substrate to evaluate the capability of AR25 to induce digestive lipase inhibition. Gastric lipase was totally inhibited by 40 mg AR25/g tributyrin whereas pancreatic lipase inhibition was maximum (78.8 +/- 0.7%) with 80 mg AR25/g tributyrin. We then used triolein, a long-chain triglyceride, to check whether AR25 could alter lipase activities on a physiologic substrate. AR25 60 mg/g triolein induced a dramatic inhibition of gastric lipase (96.8 +/- 0.4%) whereas pancreatic lipase activity was partially reduced (66.50 +/- 0.92%). Finally, the concerted action of gastric and pancreatic lipases was studied with an excess of enzymes to mimic the physiologic conditions observed in vivo. Incubation of AR25 with an excess of digestive lipases resulted in a drastic decrease in gastric lipolysis but the inhibitory effect on pancreatic lipase was less marked. On the whole, as compared to the control, lipolysis of triolein under the successive action of the two digestive lipases was reduced by 37 +/- 0.6% in the presence of AR25. Because a lipid/water interface is necessary for lipolysis to occur, lipid emulsification and emulsion droplet size were measured in gastric and duodenal media in the presence of AR25. In gastric and duodenal conditions, AR25 inhibited the lipid emulsification process. From these data we conclude that (1) in vitro, fat digestion is significantly inhibited by 60 mg AR25/g triolein, and (2) gastric as well as pancreatic lipase inhibition could be related to altered lipid emulsification in gastric or duodenal media. The green tea extract AR25 exhibiting marked inhibition of digestive lipases in vitro is likely to reduce fat digestion in humans.
PMID: 15539342 [PubMed - in process]
The green tea polyphenol (-)-epigallocatechin gallate and green tea can protect human cellular DNA from ultraviolet and visible radiation-induced damage.
Morley N, Clifford T, Salter L, Campbell S, Gould D, Curnow A.
Cornwall Dermatology Research Project, Polgooth Ward, Royal Cornwall Hospital, Treliske, Truro, Cornwall, UK.
Background: Antioxidant compounds in green tea may be able to protect against skin carcinogenesis and it is of interest to investigate the mechanisms involved. A study was therefore conducted to determine whether the isolated green tea polyphenol (-)-epigallocatechin gallate (EGCG) could prevent ultraviolet radiation (UVR)-induced DNA damage in cultured human cells. This work was then extended to investigate whether drinking green tea could afford any UVR protection to human peripheral blood cells collected after tea ingestion. Methods: The alkaline comet assay was used to compare the DNA damage induced by UVR in cultured human cells with and without the presence of EGCG. The same assay technique was then employed to assess UVR-induced DNA damage in peripheral leucocytes isolated from 10 adult human volunteers before and after drinking 540 ml of green tea. Results: Initial trials found that EGCG afforded concentration-dependent photoprotection to cultured human cells with a maximal activity at a culture concentration of 250 muM. The cells types tested (lung fibroblasts, skin fibroblasts and epidermal keratinocytes) demonstrated varying susceptibility to the UVR insult provided. The in vivo trials of green tea also demonstrated a photoprotective effect, with samples of peripheral blood cells taken after green tea consumption showing lower levels of DNA damage than those taken prior to ingestion when exposed to 12 min ultraviolet A (UVA) radiation. Conclusion: The studies showed that green tea and/or some constituents can offer some protection against UV-induced DNA damage in human cell cultures and also in human peripheral blood samples taken post-tea ingestion.
PMID: 15634219 [PubMed - in process]
Anti-obesity actions of green tea: Possible involvements in modulation of the glucose uptake system and suppression of the adipogenesis-related transcription factors.
Ashida H, Furuyashiki T, Nagayasu H, Bessho H, Sakakibara H, Hashimoto T, Kanazawa K.
Department of Biofunctional Chemistry, Faculty of Agriculture, Kobe University, Rokkodai, Nada-ku, Kobe 657-8501, Japan.
To investigate mechanisms of the anti-obesity actions of green tea in vivo, rats were given green tea instead of drinking water for 3 weeks. It was confirmed that green tea reduced adipose tissue weight without any change in body weight, other tissue weights, and food and water intakes. Green tea also significantly reduced the plasma levels of cholesterols and free fatty acids. Certain catechins existed in the plasma at 0.24 microM under our experimental conditions, though most of them existed as conjugated forms. For mechanisms of the anti-obesity actions, green tea significantly reduced glucose uptake accompanied by a decrease in translocation of glucose transporter 4 (GLUT4) in adipose tissue, while it significantly stimulated the glucose uptake with GLUT4 translocation in skeletal muscle. Moreover, green tea suppressed the expression of peroxisome proliferator-activated receptor gamma and the activation of sterol regulatory element binding protein-1 in adipose tissue. In conclusion, green tea modulates the glucose uptake system in adipose tissue and skeletal muscle and suppresses the expression and/or activation of adipogenesis-related transcription factors, as the possible mechanisms of its anti-obesity actions.
PMID: 15630268 [PubMed - in process]
