Here is some of the many Research Abstracts from the World's
leading Scientific Journals, that relate to the ingredients in
Xtreme PUMP and Backup the Science behind this amazing product.

 

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ARGININE and ORNITHINE RESEARCH

 

Title: Effect of arginine, ornithine and citrulline supplementation upon performance and metabolism of trained rats.

 

Author: Meneguello MO , Mendonça JR , Lancha AH , Costa Rosa LF

 

Source: Cell Biochem Funct, 21(1): 85-91 2003

 

Abstract: During intense exercise there is an augmented production of ammonia and IMP in the exercised muscle that could be related to the establishment of peripheral fatigue. In order to prevent this accumulation, the urea cycle in the liver eliminates ammonia in the form of urea and the skeletal muscle buffers the increase of ammonia via transamination reactions. In the present study we evaluated the effect of arginine, citrulline and ornithine supplementation, intermediates of the urea cycle, on the performance of sedentary and swimming-trained rats submitted to a single bout of exhaustive exercise. We also measured the glycogen content of the soleus and gastrocnemius muscles and of the liver, as well as the plasma concentrations of ammonia, urea, glutamine, glucose and lactate. The results indicate that arginine, citrulline and ornithine supplementation increased the flux of substrate through the reaction catalysed by glutamine synthetase, leading to increased glutamine production after an exhaustive bout of exercise, and of the mechanism involved in ammonia buffering.

 

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Title: Ornithine alpha-ketoglutarate as a potent precursor of arginine and nitric oxide: a new job for an old friend.

 

Author: Cynober L

 

Source: J Nutr, 134(10 Suppl): 2858S-2862S; discussion 2895S 2004

 

Abstract: Ornithine alpha-ketoglutarate (OKG) is a salt formed of 2 molecules of ornithine and 1 alpha-ketoglutarate. Its administration improves nutritional status in chronically malnourished (e.g., elderly) and acutely malnourished patients (especially burn and trauma patients). There is evidence that OKG activity is not the simple addition of the effects of ornithine (Orn) and alpha-ketoglutarate (alphaKG), because the presence of both moieties is required to induce the generation of key metabolites such as glutamine, proline, and arginine (Arg), whereas this does not occur when one or the other is given separately. This observation is related to the fact that the main feature of Orn at the whole-body level is to be metabolized through the Orn aminotransferase-dependent pathway, whereas the simultaneous administration of Orn and alphaKG saturates this pathway, diverting Orn toward metabolism into Arg. For years, OKG activity has been associated with its ability to induce the secretion of anabolic hormones, such as insulin and growth hormone, and to increase glutamine and polyamine synthesis. Recent studies using chemical inhibitors of nitric oxide synthase (NOS) suggest that nitric oxide derived from Arg could be partly involved in OKG activity. The use of genetically modified animals (i.e., knockout for NOS expression) is required to confirm this hypothesis.

 

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Title: Ornithine alpha-ketoglutarate supplementation influences motor activity in healthy rats

 

Author: Moinard C , Dauge V , Cynober L

 

Source: Clin Nutr, 23(4): 485-90 2004

 

Abstract: Background: Ornithine alpha-ketoglutarate (OKG) improves nutritional status in malnourished patients. Published and unpublished data suggest OKG may have effects on the central nervous system that may contribute to its action. Objective: We investigated the effect of an OKG-enriched diet on behaviour in healthy rats. Design: Thirty male Wistar rats were randomised in three groups: the OKG group was fed for 5 days (D0-D5) at 90% of spontaneous food intake with an OKG-enriched diet (5 g/kg/d). The non-essential amino acids (NEAA) group was fed similarly with a regimen enriched with NEAA (glycine, alanine, histidine and serine) to be isonitrogenous to OKG group. The ad libitum (AL) group had no treatment and was fed ad libitum with a standard regimen throughout. Rats were tested at D4 for motor activity by actimetry, and at D5 first for spontaneous alternation behaviour measured in the Y-maze, and then for exploratory behaviour measured using the open-field test (stressful environment). Results: We found that OKG supplementation enhanced global motricity by actimetry (AL 772 +/- 55, NEAA 811 +/- 54 vs. OKG 966 +/- 24 arbitrary units, P < 0.05) and total numbers of arms visited in the Y-maze (AL 26 +/- 2, NEAA 30 +/- 3 vs. OKG 38 +/- 3, P < 0.05). The lack of any effect of the OKG-enriched diet in the open-field test shows that the enhancement of locomotion activity was most probably not due to an increase in anxiety or fear in the rats. Conclusion: An OKG-enriched diet can induce beneficial stimulant effects that may be involved in the mechanism of action of OKG.

 

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Title: In vivo induction of insulin secretion by ornithine alpha-ketoglutarate: involvement of nitric oxide and glutamine.

 

Author: Schneid C , De Bandt JP , Cynober L , Torres E , Reach G , Darquy S

 

Source: Metabolism, 52(3): 344-50 2003

 

Abstract: We previously demonstrated that ornithine alpha-ketoglutarate (OKG), known for its anabolic properties, induces insulin secretion in vitro. The present study was undertaken to further characterize this effect in vivo and investigate a possible interaction with glucose both in vivo and in vitro. Male Wistar rats received an intravenous bolus of OKG (25 mg/kg) and/or glucose (0.8 g/kg) or saline, and their plasma insulin and glucose levels were monitored for 30 minutes. OKG alone increased plasma insulin to a similar extent to glucose. In combination with glucose, OKG significantly increased glucose-induced insulin secretion in vivo and in vitro, and led to a significant increase in glucose utilization in vivo. The absence of significant variations in plasma arginine and glutamine suggests a direct effect of OKG on the pancreas. To assess the involvement of the synthesis of nitric oxide and glutamine in OKG-induced insulin secretion, the experiments were repeated in the presence of inhibitors of these 2 pathways, respectively L-nitroarginine-methylester (L-NAME) and methionine sulfoximine (MSO). Both inhibitors were able significantly to reduce OKG-induced insulin secretion without affecting either basal or glucose-induced insulin release. Thus OKG acts directly with glucose on islets to induce insulin secretion via mechanisms involving NO and glutamine synthesis. In addition, our results suggest that OKG and glucose act via separate pathways.

 

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Title: Action of ornithine alpha ketoglutarate on DNA synthesis by human fibroblasts.

 

Author: Vaubourdolle M , Salvucci M , Coudray-Lucas C , Agneray J , Cynober L , Ekindjian OG

 

Source: In Vitro Cell Dev Biol, 26(2): 187-92 1990

 

Abstract: Ornithine alpha ketoglutarate (OKG) is largely used in clinical nutrition for its anabolic effects. However, the mechanism of its action remains questionable. We investigated the effect of OKG on the rate of DNA synthesis in human fibroblasts. The in vitro experimental procedure required to demonstrate in cell culture the anabolic effects of OKG observed in vivo was found to be glutamine-free and serum-poor medium with sparse cells. In these conditions, OKG induced a significant increase in [3H]thymidine incorporation compared to untreated control cells. This effect was dose-dependent and was observed in all the cultures tested. Taken individually, the two constituents of OKG, i.e. alpha KG and Orn, also showed a stimulatory effect, but did not demonstrate a dose-dependent response. Concomitant analysis of extracellular aminoacids showed in alpha KG-treated cultures an increase in glutamate and a decrease in aspartate, suggesting a cellular transamination of alpha KG. Glutamine, which is the preferential energetic substrate of fibroblasts, can be produced from glutamate and might play a role in the action of OKG. Moreover, OKG induced a rise in the cellular polyamine content. This, in association with the inhibitory effect on OKG action of difluoromethylornithine, a specific inhibitor of ornithine decarboxylase, suggests a link between the polyamine biosynthesis pathway and the anabolic effect of OKG.

 

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Title: Glutamine and ornithine-alpha-ketoglutarate but not branched-chain amino acids reduce the loss of muscle glutamine after surgical trauma.

 

Author: Wernerman J , Hammarkvist F , Ali MR , Vinnars E

 

Source: Metabolism, 38(8 Suppl 1): 63-6 1989

 

Abstract: The concentration of free glutamine in skeletal muscle decreases characteristically after surgical trauma. In animal studies a correlation between muscle protein synthesis and the glutamine concentration is reported. For pharmaceutical reasons, commercially available amino acid solutions do not contain glutamine. Therefore, at present, postoperative total parenteral nutrition does not provide glutamine. Several modifications of the composition of the amino acid solutions given in total parenteral nutrition have been evaluated recently. Ornithine-alpha-ketoglutarate preserves muscle protein synthesis and spares nitrogen after elective surgery, and an extra supply of branched-chain amino acids improves muscle protein synthesis in animals. Patients undergoing elective abdominal surgery (n = 33) received isocaloric (135 kJ/kg body weight/24 h) and isonitrogenous (0.2 g N/kg body weight/24 h) total parenteral nutrition for three days immediately following surgery. Administration of glutamine and ornithine-alpha-ketoglutarate as part of the amino acid supply reduced the loss of muscle glutamine from 40% to 25% (P less than .05). Additional supplementation of branched-chain amino acids produced no such effect, however, as compared with the control group.

 

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NADH RESEARCH

References

1. Kuhn W, Muller T, Winkel R, et al. Parenteral application of NADH in Parkinson’s disease: clinical improvement partially due to stimulation of endogenous levodopa biosynthesis. J Neural Transm 1996;103:1187–93.

2. Birkmayer W, Birkmayer JGD, Vrecko K, et al. The clinical benefit of NADH as stimulator of endogenous L-Dopa biosynthesis in Parkinsonian patients. In: Streifler MB, Korczyn AD, Melamed E, et al. (eds). Advances in Neurology, vol. 53 (Parkinsons Disease: Anatomy, Pathology, and Therapy). New York: Raven Press, 1990, 545–9.

3. Birkmayer JG, Vrecko C, Volc D, Birkmayer W. Nicotinamide adenine dinucleotide (NADH)— a new therapeutic approach to Parkinson’s disease. Comparison of oral and parenteral application. Acta Neurol Scand Supp 1993;146:32–5.

4. Dizdar N, Kagedal B, Lindvall B. Treatment of Parkinson’s disease with NADH. Acta Neurol Scand 1994;90:345–7.

5. Birkmayer JG. Coenzyme nicotinamide adenine dinucleotide: new therapeutic approach for improving dementia of the Alzheimer type. Ann Clin Lab Sci 1996;26:1–9.

6. Birkmayer JGD, Birkmayer W. The coenzyme nicotinamide adenine dinucleotide (NADH) as biological antidepressive agent: experience with 205 patients. New Trends Clin Neuropharmacol 1991;5:19–25.

7. Forsyth LM, MacDowell-Carnciro AL, Birkmayer GD, et al. The use of NADH as a new therapeutic approach in chronic fatigue syndrome. Presented at the annual meeting of the American College of Allergy, Asthma & Immunology, 1998.

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