From:
sukiec@optonline.net
Date: 2005-09-23 20:44:26 UTC
Subject: RE: Can Melatonin implants cause inolinoma?
To: ferrethealth@smartgroups.com
Message-ID: <3726731.1127508266188.JavaMail.root@thallium.smartgroups.com>
I suspect that your sister's friend was confused, but I certainly could be =
wrong.
This was a multi-part study. Notice an opposite effect of what was reporte=
d to you.
START QUOTE
J Pineal Res. 2002 Sep;33(2):63-71.
Related Articles, Links
=
Receptor (MT(1)) mediated influence of melatonin on cAMP concentration and =
insulin secretion of rat insulinoma cells INS-1.
Peschke E, Muhlbauer E, Musshoff U, Csernus VJ, Chankiewitz E, Peschke D.
Institute of Anatomy and Cell Biology, Martin-Luther-University Halle-Witte=
nberg, Halle/Saale, Germany. elmar.peschke@medizin.uni-halle.de
Recent functional, autoradiographic, and molecular investigations have show=
n that the pineal secretory product melatonin reduces the forskolin-stimula=
ted insulin secretion from isolated pancreatic islets of neonate rats. =
...
In order to examine this question, we used a glucose responsive insulin pr=
oducing insulinoma cell line INS-1 isolated from rats. Comparable with the =
results of islets the competitive receptor antagonist luzindole diminished =
the insulin-decreasing effect of melatonin. =
...
From these data we conclude that the MT1 receptor is located on the INS-1 =
cell and therefore in general on pancreatic beta-cells.
PMID: 12153439 [PubMed - indexed for MEDLINE]
END QUOTE
This is a more recent study, and honestly someone with more endocrinology t=
han I had better interpret what if anything it might mean in relation to in=
sulinoma:
START QUOTE
J Pineal Res. 2005 Oct;39(3):316-23.
Related Articles, Links
=
Melatonin stimulates inositol-1,4,5-trisphosphate and Ca release from INS1 =
insulinoma cells.
Bach AG, Wolgast S, Muhlbauer E, Peschke E.
Institute of Anatomy and Cell Biology, Martin Luther University Halle-Witte=
nberg, Halle/Saale, Germany.
The effects of melatonin in mammalian cells are exerted via specific recept=
ors or are related to its free radical scavenging activity. It has previous=
ly been reported that melatonin inhibits insulin secretion in the pancreati=
c islets of the rat and in rat insulinoma INS1 cells via G(i)-protein-coupl=
ed MT1 receptors and the cyclic adenosine 3',5'-monophosphate pathway. Howe=
ver, the inositol-1,4,5-trisphosphate (IP(3)) pathway is involved in the in=
sulin secretory response as well, and the melatonin signal may play a part =
in its regulation. This paper addresses the involvement of the second messe=
ngers IP(3) and intracellular Ca(2+) ([Ca(2+)](i)) in the signalling cascad=
e of melatonin in the rat insulinoma INS1 cell, a model for the pancreatic =
beta-cell. For this purpose melatonin at concentrations ranging from 1 to 1=
00 nmol/L, carbachol and the nonselective melatonin receptor antagonist luz=
indole were used to stimulate INS1 cell batches, followed by an IP(3)-mass =
assay and Ca(2+) imaging. Molecular biological studies relating to the mRNA=
of IP(3) receptor (IP(3)R) subtypes and their relative abundance in INS1 c=
ells showed expression of IP(3)R-1, IP(3)R-2 and IP(3)R-3 mRNA. In conclusi=
on, we found that in rat insulinoma INS1 cells there is a dose-dependent st=
imulation of IP(3) release by melatonin, which is accompanied by a likewise=
transient increase in [Ca(2+)](i) concentrations. The melatonin effect obs=
erved mimics carbachol action. It can be abolished by 30 mumol/L luzindole =
and is sustained in Ca(2+)-free medium, suggesting a mechanism that include=
s the depletion of Ca(2+) from intracellular stores.
END QUOTE
The following 1999 article (available in full on line at
http://www.jneurosci.org/cgi/content/full/19/1/206 ) *may* be related to so=
me degree. =
START QUOTE
The Journal of Neuroscience, January 1, 1999, 19(1):206-219
Pituitary Adenylate Cyclase-Activating Polypeptide and Melatonin in the Sup=
rachiasmatic Nucleus: Effects on the Calcium Signal Transduction Cascade
Michael D. A. Kopp1, 2, Christof Schomerus1, Faramarz Dehghani1, Horst-Wern=
er Korf1, and Hilmar Meissl2
1 Dr. Senckenbergische Anatomie, Anatomisches Institut II, Johann Wolfgang =
Goethe-Universit=E4t, D-60590 Frankfurt, Germany, and 2 Max-Planck-Institut=
f=FCr Physiologische und Klinische Forschung, W. G. Kerckhoff-Institut, D-=
61231 Bad Nauheim, Germany
END QUOTE
A 2003 dissertation that investigates an inflammation question:
http://www.diva-portal.org/diva/getDocument?urn_nbn_se_uu_diva-3537-1__full=
text.pdf
(It looks at nitric oxide and melatonin in relation to Beta cell sensitivit=
y to cytokines.)
This has some intriguing abstracts on too much light exposure, malignancies=
, and neurodegenerative diseases:
http://www.nel.edu/Press/Light-Endocrine-Cancer.htm
http://www.jpp.krakow.pl/journal/archive/0604_s2/articles/03_article.html
START QUOTE
A. LEJA-SZPAK1, J. JAWOREK1, K. NAWROT-PORABKA1, M. PALONEK1,
M. MITIS-MUSIOL2, A. DEMBINSKI2, S.J. KONTUREK2, W.W. PAWLIK2
MODULATION OF PANCREATIC ENZYME SECRETION BY MELATONIN AND ITS =
PRECURSOR; L-TRYPTOPHAN. ROLE OF CCK AND AFFERENT NERVES.
Dept Med Physiol Faculty of Health Care1 and Chair of Physiology Med Facult=
y2 Jagiellonian University Collegium Medicum, Cracow, Poland
=
Melatonin, a pineal hormone, is also produced in the gastrointestinal tract=
. Melatonin receptors have been detected in the stomach, intestine and panc=
reas. This indole inhibits insulin secretion but its role in the physiologi=
cal modulation of exocrine pancreatic function is yet unknown. The aim of t=
his study was to evaluate the pancreatic secretory effect of melatonin and =
its precursor; L-tryptophan given intraduodenally (i.d.) to the conscious r=
ats with intact or capsaicin deactivated sensory nerves. CCK1 receptor anta=
gonist; tarazepide, was used in the part of the study to determine the invo=
lvement of CCK in the secretory effects of melatonin. The secretory studies=
were performed on awaken rats surgically equipped with silicone catheters,=
one of them was inserted into pancreato-biliary duct, the other one - into=
duodenum. Melatonin (1, 5 or 25 mg/kg) or L-tryptophan (10, 50 or 250 mg/k=
g) were administered i.d. Samples of pancreatic juice were collected in 15 =
minutes aliquots. Tarazepide (2,5 mg/kg i.p.) was given to the rats 15 min =
prior to the administration of melatonin or L-tryptophan. Neurotoxic dose o=
f capsaicin (100 mg/kg s.c.) was used to deactivate afferent nerves and thu=
s to assess the role of these nerves in the melatonin-induced pancreatic en=
zyme secretion. Administration of melatonin (1, 5 or 25 mg/kg i.d.) or L-tr=
yptophan (10, 50 or 250 mg/kg i.d.) significantly increased pancreatic amyl=
ase outputs. Deactivation of sensory nerves by capsaicin or administration =
of CCK1 - receptor antagonist; tarazepide, reversed the stimulatory effects=
of melatonin or L-tryptophan on pancreatic secretory function. Administrat=
ion of melatonin or its amino-acid precursor to the rats resulted in the si=
gnificant and dose-dependent rises of melatonin and CCK plasma levels. We c=
onclude that melatonin or its precursor; L-tryptophan stimulates pancreatic=
enzyme secretion via stimulation of CCK release and activation of duodeno-=
pancreatic reflexes.
Key words:
melatonin, L-tryptophan, pancreatic enzyme secretion, tarazepide, sensory n=
erves
END QUOTE
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