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DAA gali padidinti prolaktino lygi

"Endocrinology. 2000 Oct;141(10):3862-70.
The role of D-aspartic acid and N-methyl-D-aspartic acid in the regulation of prolactin release.
D'Aniello G, Tolino A, D'Aniello A, Errico F, Fisher GH, Di Fiore MM.
Source

Laboratory of Neurobiology, Zoological Station of Naples, Italy.
Abstract

In this study, using an enzymatic HPLC method in combination with D-aspartate oxidase, we show that N-methyl-D-aspartate (NMDA) is present at nanomolar levels in rat nervous system and endocrine glands as a natural compound, and it is biosynthesized in vivo and in vitro. D-aspartate (D-Asp) is its natural precursor and also occurs as an endogenous compound. Among the endocrine glands, the highest quantities of D-Asp (78 +/- 12 nmol/g) and NMDA (8.4 +/- 1.2 nmol/g) occur in the adenohypophysis, whereas the hypothalamus represents the area of the nervous system where these amino acids are most abundant (55 +/- 9 and 5.6 +/- 1.1 nmol/g for D-Asp and NMDA, respectively). When D-Asp is administered to rats by ip injection, there is a significant uptake of D-Asp into the adenohypophysis and a significant increase in the concentration of NMDA in the adenohypophysis, hypothalamus and hippocampus, suggesting that D-Asp is an endogenous precursor for NMDA biosynthesis. Experiments conducted on tissue homogenates confirm that D-Asp is the precursor of the NMDA and that the enzyme catalyzing this reaction is a methyltransferase. S-adenosyl-L-methionine (SAM) is the methyl group donor. In vivo experiments consisting of ip injections of sodium D-aspartate show that this amino acid induced a significant serum PRL elevation and this effect is dose and time dependent. In vitro experiments conducted on isolated adenohypophysis or adenohypophysis coincubated with the hypothalamus, showed that the release of PRL is caused by a direct action of D-Asp on the pituitary gland and also mediated by the indirect action of NMDA on the hypothalamus. Then, the latter induces the release of a putative factor that in turn stimulates the adenohypophysis reinforcing the PRL release. In conclusion, our data suggest that D-Asp and NMDA are present endogenously in the rat and are involved in the modulation of PRL release."

Saltinis:
http://www.ncbi.nlm.nih.gov/pubmed/11014243

Geras daiktas DAA, prie PCT jauciasi ypac vienintelis efektyvus test boosteris koki bandes

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Paskutinį kartą taisė Artyi (2013-12-17 12:48)

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Paskutinį kartą taisė Artyi (2013-12-17 12:48)

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Paskutinį kartą taisė Artyi (2013-12-17 12:48)

D-Aspartic Acid not effective in young bodybuilders

You're in your early twenties, and you're looking for a supplement that will boost your testosterone level and thus speed up your muscle bulking. Whatever you do, don't try D-aspartic acid. According to a small human study published by sports scientists Darryn Willoughby and Brian Leutholtz in Nutrition Research, the effect of D-aspartic acid on testosterone levels is minimal and the same goes for its effect on muscle strength.

After an Italian study showed that supplementation with 3 g sodium-D-aspartate boosted testosterone levels in elderly men, D-aspartic acid analogues became a modest rage in the sports supplements world. Experiences with pure D-aspartic acid were not particularly hopeful; those with calcium and sodium salts of the amino acid were better. The body absorbs these forms of D-aspartic acid better.

Willoughby and Leutholtz were sceptical about the D-aspartic acid rage. The men in the Italian study had low testosterone levels while bodybuilders generally have a high level as a result of heavy physical training and carefully worked out diets. So is D-aspartic acid effective in this group?

This is the question the researchers tried to answer by doing a 28-day long experiment with 20 recreational bodybuilders whose average age was 22.

The researchers gave half of their subjects 3 g D-aspartic acid daily. The other half of the subjects were given a placebo.

The supplement didn't work. The tables below show that the increases in testosterone level and strength were negligible. The effects were not significant at all.







The researchers observed that the supplementation only resulted in a limited rise in the subjects' D-aspartic acid level. What had risen significantly was the level of the enzyme D-aspartate oxidase – an enzyme that breaks down D-aspartic acid in the intestines, kidneys and liver.

So D-aspartic acid doesn't work, the researchers sum up. "We conclude that 28 days of D-aspartic acid supplementation at a daily dose of 3 g is ineffective in upregulating the activity of the hypothalamo-pituitary-gonadal axis and has no preferential effects in which to increase skeletal muscle mass and strength in resistance-trained men", they write.

This is the case for the free form of D-aspartic acid. The study has little to say when it comes to the sodium and calcium bound analogues of D-aspartic acid, sodium-D-aspartate and calcium-D-aspartate.

Source:
Nutrition Research. Available online 15 August 2013.


Saltinis: ergo-log.com

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Tai jau ir sitas neveikiantis. Robse, help, mums reik alternatyvuuu

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