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[A1CR]

What Oleoylethanolamide (OEA) is may be explained by
http://tinyurl.com/ymgmte http://tinyurl.com/yz89y3 sites.
As a further introductions to a new CR paper, which appears
to address what happens biochemically in our brains that can
cause CR, see: http://tinyurl.com/3n982 and
http://tinyurl.com/5e8sm in which there is discussion of a
cannabinoid agent that is natural and causes CR. It is
called, apparently, oleylethanolamide or oleoylethanolamide
(OEA). Also for introduction, see the below excerpts from
an available free full-text that has not been described on
this forum previously and does also present relevant
findings independently on what the biochemicals in our own
bodies may do to affect our CR.

Cani PD, Montoya ML, Neyrinck AM, Delzenne NM, Lambert DM.
Potential modulation of plasma ghrelin and glucagon-like
peptide-1 by
anorexigenic cannabinoid compounds, SR141716A (rimonabant) and
oleoylethanolamide.
Br J Nutr. 2004 Nov;92(5):757-61.
PMID: 15533263

The CB1 cannabinoid receptor antagonist,
N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3-carboxamide

(rimonabant; SR141716A), and oleoylethanolamide (OEA) are
known to reduce
food consumption, by, at least partially, a peripheral
regulation of
feeding. The effects of systemic SR141716A or OEA (5 mg/kg)
administrations
on food consumption in 24 h food-deprived and fed rats were
investigated. In
fasted rats, SR141716A and OEA produced an inhibition in
food intake
measurable the first 20 min following injection. The
increase in ghrelin
levels observed in the vehicle-injected rats was abolished
in animals
receiving OEA and significantly reduced with SR141716A.
Neither OEA nor
SR141716A modified glucagon-like peptide-1 (7-36) amide
portal levels 20 min
after the administration. In fed rats, plasma ghrelin levels
of SR141716A-
and OEA-treated rats were 35% lower as compared with those
of the
vehicle-injected rats. These results show an influence of
cannabinoid agents
on circulating ghrelin levels and suggest that their
short-term action on
appetite seems to be in accordance with the control of
secretion of
gastrointestinal orexigenic peptides, mainly expressed in
the upper part of
the gastrointestinal tract.

... In conclusion, there is now increased evidence for a
peripheral role of
the cannabinoid system in food-consumption behaviour;
however, the molecular
mechanisms allowing the different cannabinoid-related
molecules to act on
food intake through their action on the gastrointestinal
tract remain to be
fully elucidated. Although interactions between cannabinoid
and ghrelin
signalling pathways have been recently suggested in the
regulation of food
intake by the brain-gut axis (Konturek et al. 2004), it is
too early to
anticipate with the present data the precise molecular basis
of such a
potential interaction. We have shown that the peripheral
administration of
SR141716 maintains ghrelin plasma levels at a lower level,
which is in
'concordance' with the rapid decrease of food intake
observed after its
peripheral administration. The peripheral administration of
OEA shows also a
tendency to decrease this level compared with the vehicle,
confirming the
role of this analogue of AEA as an anorexigenic endogenous
mediator. The
cannabinoid system interacts with several peptides involved
in the complex
regulation of energy homeostasis such as leptin (Di Marzo et
al. 2001), Acrp
30 (Bensaid et al. 2003) and orexin (Cota et al. 2003b;
Hilairet et al.
2003). The present study suggests that the modulation of the
secretion of
gastrointestinal orexigenic peptides, such as ghrelin, by
the cannabinoid
system, mainly expressed in the upper part of the
gastrointestinal tract,
may participate in food regulation.

And, now, here is the pdf available Medline abstract of a
fairly recent CR
paper that is free full-text to all.

Wang X, Miyares RL, Ahern GP.
Oleoylethanolamide excites vagal sensory neurones, induces
visceral pain and
reduces short-term food intake in mice via capsaicin
receptor TRPV1.
J Physiol. 2005 Apr 15;564(Pt 2):541-7. Epub 2005 Feb 3.
PMID: 15695242

Oleoylethanolamide (OEA) is an endogenous lipid that
regulates feeding and
body weight. Although the effects of OEA are believed to
depend on
activation of vagal sensory afferent neurones, the
mechanisms involved in
exciting these neurones are unclear. Here we show that OEA
directly excited
nodose ganglion neurones, the cell bodies of vagal
afferents. OEA
depolarized these neurones and evoked inward currents that
were restricted
to capsaicin-sensitive cells. These currents were fully
blocked by the TRPV1
inhibitor, capsazepine, and no responses to OEA were
observed in neurones
cultured from TRPV1-null mice. Similarly, OEA induced a rise
in Ca(+)
concentration in wild-type but not TRPV1-deficient neurones,
and responses
to OEA were greater at 37 degrees C compared to room
temperature.
Significantly, OEA administration in mice induced visceral
pain-related
behaviours that were inhibited by capsazepine and absent in
TRPV1-null
animals. Further, OEA reduced 30-min food intake in
wild-type but not in
TRPV1-null mice. Thus, the acute behavioural effects of OEA
may result from
visceral malaise via the activation of TRPV1.

A current paper below describing how CRing and refeeding may
involve OEA .

Fu J, Astarita G, Gaetani S, Kim J, Cravatt BF, Mackie K,
Piomelli D.
Food intake regulates oleoylethanolamide formation and
degradation in the
proximal small intestine.
J Biol Chem. 2006 Nov 22; [Epub ahead of print]
PMID: 17121838

Oleoylethanolamide (OEA) is a lipid mediator that inhibits
food intake by
activating the nuclear receptor peroxisome
proliferator-activated receptor-a
(PPAR-a). In the rodent small intestine, OEA levels decrease
during food
deprivation and increase upon refeeding, suggesting that
endogenous OEA may
participate in the regulation of satiety. Here we show that
feeding
stimulates OEA mobilization in the mucosal layer of rat
duodenum and
jejunum, but not in the serosal layer from the same
intestinal segments, in
other sections of the gastrointestinal tract (stomach,
ileum, colon), or in
a broad series of internal organs and tissues (e.g., liver,
brain, heart,
plasma). Feeding also increases the levels of other
unsaturated fatty-acid
ethanolamides (FAEs) (e.g., linoleoylethanolamide) without
affecting those
of saturated FAEs (e.g., palmitoylethanolamide).
Feeding-induced OEA
mobilization is accompanied by enhanced accumulation of
OEA-generating
N-acyl phosphatidylethanolamines (NAPEs), increased activity
and expression
of the OEA-synthesizing enzyme NAPE-phospholipase D
(NAPE-PLD), and
decreased activity and expression of the OEA-degrading
enzyme fatty-acid
amide hydrolase (FAAH). Immunostaining studies revealed that
NAPE-PLD and
FAAH are expressed in intestinal enterocytes and lamina
propria cells.
Collectively, these results indicate that nutrient
availability controls OEA
mobilization in the mucosa of the proximal intestine through
a concerted
regulation of OEA biosynthesis and degradation.