Supplement Direct N-Acetyl L-Glutamine 250 Grams

N-Acetyl-L-Glutamine (Aceglutamite or NAG�) is known in foreign countries as an anti-ulcer drug that works by forming a protective layer over the lining of the stomach. It accomplishes this by activating a chemical action that serves as an anti-acid buffer while suppressing the secretion of pepsin, a protein-digesting enzyme produced in the stomach.

More recent clinical research indicates Aceglutamide to be a psycho stimulant while improving memory and the ability to concentrate in persons showing signs of senile dementia. Chemically speaking, N-Acetyl-L-Glutamine is the acetylated version of the most abundant amino acid found in skeletal muscle tissue, which is glutamine. is more stable in water and metabolically efficient at delivering glutamine�s biological effects over conventional Glutamine or Glutamine Peptides. N-Acetyl-L-Glutamine will also play a dominant role in increasing muscle cell volume, glycogen storage, and growth hormone production while simultaneously supporting ones own immune system function. N-Acetyl-L-Glutamineis an extremely versatile compound with a plethora of research that warrants its use in athletes besides of what it is used for in clinical nutrition. The optimal dosage range is in the neighborhood of around 1-5 grams per day taken on an empty stomach.

Absorption of enterally administered N-acetyl-l-glutamine versus glutamine in pigs.

Arnaud A, Ramirez M, Baxter JH, Angulo AJ.

Abbott Laboratories, Ross Products Division, International R and D Department, Camino de Purchil 68, Granada 18004, Spain.

BACKGROUND AND AIMS: Glutamine instability in liquid media suggests that evaluation of reasonable enteral nutrition sources of glutamine is needed. N-acetyl-l-glutamine offers no instability and no intolerance problems. This research was conducted to study the absorption and apparent digestibility of glutamine versus N-acetyl-l-glutamine. METHODS: Two pig models were used. (1) In a clamped jejunal loop experiment, we measured the concentrations of glutamine and N-acetyl-l-glutamine in the intestinal infused solutions, intestinal mucosa, and portal and peripheral blood. (2) In a feeding experiment, we determined their apparent digestibility. RESULTS: N-acetyl-l-glutamine ( approximately 76%) was slightly less absorbed than glutamine ( approximately 85%) from the intestinal lumen into mucosa, where it was not detected as intact molecule, suggesting almost complete hydrolysis during absorption. Virtually no intact N-acetyl-l-glutamine was observed in the blood compartments; glutamine from lumenal N-acetyl-l-glutamine had the same behavior as that from lumenal-free glutamine in portal and peripheral blood. The apparent ileal digestibility of N-acetyl-l-glutamine was lower than that of free glutamine, as N-acetyl-l-glutamine was probably retained in the intestinal lumen to a greater extent than glutamine. CONCLUSION: N-acetyl-l-glutamine appeared to be a good candidate for glutamine fortification of enteral nutrition formulas.

NMR and MS analysis of decomposition compounds produced from N-acetyl-L-glutamine at low pH.

Bergana MM, Holton JD, Reyzer IL, Snowden MK, Baxter JH, Pound VL.

Ross Products Division, Abbott Laboratories, 625 Cleveland Avenue, Columbus Ohio 43215, USA. marti.bergana@rossnutrition.com

N-Acetyl-L-glutamine decomposition products glutamine, glutamic acid, pyroglutamic acid, N-acetylglutamic acid, and a novel compound, N-(2,6-dioxo-3-piperidinyl) acetamide, have been identified by NMR and MS techniques. N-Acetylglutamine, a modified amino acid, offers greater chemical stability than glutamine in conditions that are experienced during typical sterilization and shelf storage of liquid nutritionals. However, to support safety and stability studies, potential decomposition products of N-acetyl-L-glutamine needed to be identified. Therefore, atypically harsh conditions were used; an unbuffered (pH <3) 1 mg/mL water solution of N-acetyl-L-glutamine was heated to 100 degrees C for 3 h. One-dimensional proton and proton-decoupled carbon-13 NMR and electrospray LC-MS/MS techniques were employed to identify the molecular structures of the generated N-acetyl-L-glutamine decomposition products. Additionally, DEPT and two-dimensional NMR techniques TOCSY, GMQCOSY, GHSQC, and GHMBC were employed to derive the final structure of the acetamide.

Memory deficits of aged male rats can be improved by pyrimidine nucleosides and n-acetyl-glutamine.

Drago F, D'Agata V, Valerio C, Spadaro F, Raffaele R, Nardo L, Grassi M, Freni V.

Institute of Pharmacology, University of Catania Medical School, Italy.

The pyrimidine nucleosides uridine (URI) and cytidine (CYT), alone or associated with n-acetyl-glutamine (NAG), were injected acutely or subchronically to aged (26 months old) male rats of the Sprague-Dawley strain. Learning and memory abilities of the animals were studied with tests of avoidance behavior. The acquisition of active avoidance behavior was studied with the shuttle-box test. A step-through type of passive avoidance task was used to examine the retention of passive avoidance responses. The acquisition of the active avoidance behavior and the retention of the passive avoidance response were reduced in aged animals as compared with those of young animals. Neither the acute treatment of old rats with URI and CYT alone nor that associated with NAG exerted any effect on the behavioral tests. In contrast, the subchronic treatment with URI and CYT was followed by a facilitation of acquisition of active avoidance behavior in the shuttle box and of retention of passive avoidance responses in the dark box. A more potent effect on the acquisition of the shuttle-box behavior and on the retention of passive avoidance reaction was found in animals treated subchronically with the pyrimidine nucleosides associated with NAG. These effects may be related to the role of pyrimidines in the synthesis of ribonucleic acid, which is indispensable for learning and memory processes.

Effect of N-acetyl-L-glutamine aluminum complex (KW-110), an antiulcer agent, on the non-steroidal anti-inflammatory drug-induced exacerbation of gastric ulcer in rats.

Tanaka H, Shuto K, Marumo H.

Gastric ulcer induced by the injection of acetic acid (0.025 ml of 20%) into the gastric wall of rats was healed considerably 5 days after the injection of acetic acid. Non-steroidal anti-inflammatory drugs (NSAID) such as aspirin, indomethacin, and phenylbutazone were given consecutively for 5 days, and they exacerbated the ulcer and enlarged the ulcer area. Aspirin caused exacerbation when it was given for the initial 5 days of the ulcer healing process. Phenylbutazone caused exacerbation by the administration for 5 days at the middle stage of the ulcer healing process. In contrast, indomethacin caused exacerbation not only when it was given for the initial 5 days but also when it was given for the middle 5 days. The effect of the antiulcer agent N-acetyl-L-glutamine aluminum complex (KW-110) on the exacerbation was studied. KW-110 at an oral dose of 500 mg/kg inhibited remarkably the exacerbation induced by all of the NSAID used. The development of gastric lesions induced by these NSAID was also prevented by KW-110. Further study was carried out with regard to the influences of KW-110 on the pharmacological properties of NSAID. The results showed no influences of KW-110 on the antiedematous and antipyretic actions of the NSAID.