Glutamine (Gln) is the most abundant free amino acid
in the body and plays a vital role in amino acid transport
and nitrogen balance. Gln is also a primary fuel for
rapidly dividing cells such as enterocytes and lymphocytes,
which protect mucosa barricade and enhance immune functions[1].
Patients undergoing elective abdominal surgery usually
have malnutrition and Gln concentration is low in blood
due to several factors: mechanical obstruction, limitation
of food intake, tumor-induced cachexia, obstruction
of pancreaticobiliary, malabsorption and ongoing blood
loss. Moreover, intravascular and free muscle glutamine
pools become depleted in response to perioperative abrosia
and operative stress. Free Gln is lack of stability
in solution and intravenous adminitration is limited.
Glutamine dipeptide (L-alanyl-L-glutamine) can be taken
via vein and hydrolyzed into glutamine in circulation
as Gln substitution. It was given to patients undergoing
abdominal surgery in order to improve their postoperative
nitrogen balance and immunonutrition[2]. Therefore,
it is worth knowing whether routine supplementation
of glutamine dipeptide in parenteral nutrition (PN)
can amend clinical outcomes. Meta-analysis has been
applied in medical research to improve statistical effi
ciency, to evaluate the disadvantage of established
studies and to draw reliable conclusions from various
potentially relevant studies. It is the most promising
approach for future research and a guideline for clinical
treatment[3]. This meta-analysis aims to enhance our
understanding of the clinical and economical validity
of glutamine dipeptide for patients undergoing abdominal
surgery. (http://www.wjgnet.com/)
The objective of this research is to test the hypothesis that glycyl-
L-glutamine, a dipeptide synthesized through the post-translational processing
of Beta-endorphin, acts as a neurotransmitter in brain and a circulating hormone
in the periphery. To test this hypothesis, we established three working
objectives: (1) to evaluate the physiological responses produced by glycyl L
glutamine and test whether it modulates the opiate actions of Beta-endorphin;
(2) to examine its distribution in brain and pituitary and determine whether it
is specifically co-localized with Beta-endorphin; (3) to characterize the
receptors which mediate glycyl L glutamine's pharmacologic effects. During the
current project period, we found that glycyl L glutamine produces three markedly
different pharmacologic responses: it stimulates a trophic response in cardiac
myocytes, inducing expression of the asymmetric form of acetylcholinesterase, a
classical marker for synaptic innervation; it produces neuroimmune regulatory
effects in T lymphocytes, enhancing c-myc oncogene expression. (http://oai.dtic.mil/)
Glycyl-glutamine (Gly-Gln) is an inhibitory dipeptide
synthesized from β-endorphin1–31. Previously, we showed
that Gly-Gln inhibits morphine conditioned place preference,
tolerance, dependence and withdrawal. In this study,
we tested whether Gly-Gln's inhibitory activity extends
to other rewarding drugs, specifically nicotine. Rats
were conditioned with nicotine (0.6 mg/kg, s.c.) for
four days and tested on day five. Glycyl-glutamine (100
nmol i.c.v.) inhibited acquisition and expression of
a nicotine place preference significantly. Cyclo(Gly-Gln)
(100 nmol i.c.v. or 25 mg/kg i.p.), a cyclic Gly-Gln
derivative, blocked expression of nicotine place preference
but Gly-D-Gln (100 nmol i.c.v.) was ineffective. To
study nicotine withdrawal, rats were treated with nicotine
(9 mg/kg/day) for seven days and conditioned place aversion
was induced with mecamylamine (1 mg/kg, s.c.). Glycyl-glutamine
blocked acquisition of place aversion to mecamylamine
but not U50,488, a kappa opioid receptor agonist. Glycyl-glutamine
thus inhibits the rewarding effects of nicotine and
attenuates withdrawal in nicotine dependent rats. (http://farmakoloji.uludag.edu.tr/)
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