From:
"Sukie Crandall"
Date: 2007-01-28 19:55:35 UTC
Subject: [ferrethealth] Re: white poo and cetera followup
To: ferrethealth@yahoogroups.com
Have CBC and a Chemistry Panel (blood tests) done.
IBD and stomach inflammation can also cause inflammation of the liver and s=
ometimes of
the pancreas.
Either an inflamed pancreas or an inflamed liver can result in the bilirubi=
n not reaching the
intestine.
That means a pack of pigment in the feces.
Having bile not reach the intestine also causes other problems, including m=
aking the
intestine more vulnerable to infection:
http://www.eurekalert.org/pub_releases/2006-02/usmc-gpf020306.php
It is also important to remember that the small intestine has a feedback lo=
op on bile
production so IBD could throw that off:
http://www.eurekalert.org/pub_releases/2005-10/usmc-flf101005.php
Both of those are short and highly informative research press releases so I=
might as well
just carry them here:
BEGIN QUOTES
Public release date: 6-Feb-2006
Contact: Aline McKenzie
aline.mckenzie@utsouthwestern.edu
214-648-3404
UT Southwestern Medical Center
Gut protein found to protect against infection and intestinal breakdown
A protein that binds to bile in the small intestine may hold the key to pre=
venting infection
and intestinal breakdown in people with conditions such as obstructive jaun=
dice or
irritable bowel syndrome, researchers at UT Southwestern Medical Center hav=
e discovered.
"What we've identified is one of the mechanisms for how the body keeps the =
number of
bacteria low in the small intestine, and how it prevents them from getting =
into other
organs," said Dr. Steven Kliewer, professor of molecular biology, senior au=
thor of the study
and holder of the Nancy B. and Jake L. Hamon Distinguished Chair in Basic C=
ancer
Research. The study is available this week online and in an upcoming issue =
of the
Proceedings of the National Academy of Sciences.
Bile, which is generated by the liver and flows into the small intestine vi=
a a duct, contains
harsh acids that help the body absorb nutrients, kill certain bacteria and =
help keep intact
the lining of the intestine, a major barrier against the infiltration of in=
fectious
microorganisms. That's no small task; if the innermost lining of the small =
intestine alone
were unfolded, it would be the size of a tennis court.
When there's no bile in the intestine, as happens in people with obstructiv=
e jaundice or in
those who rely on feeding tubes for nourishment, the lining breaks down and=
bacteria
pass through it into the body, sometimes causing the massive blood infectio=
n known as
sepsis. Simply giving bile acids orally as a substitute isn't a good soluti=
on because they
can cause liver damage, Dr. Kliewer said.
The researchers focused on a molecule =96 FXR =96 in the wall of the lining=
, which binds to bile
acids. When FXR was activated by a synthetic binding chemical called GW4064=
, it was
found to activate several genes that are known to protect the intestinal li=
ning or attack
bacteria.
The research team also found that FXR molecules heavily lined the inside fo=
lds of the
intestine in adult mice.
"It's perfectly positioned," Dr. Kliewer said. "It's expressed in just the =
right place to protect
us from the environment."
When the bile ducts of mice were tied off, preventing bile from reaching th=
e intestine,
adding GW4064 prevented damage to the intestines, showing that it can repla=
ce bile in
protecting the small intestine.
Genetically engineered mice that lacked FXR showed overall damage to the in=
testines,
"strong evidence that this protein is crucial," Dr. Kliewer said. Drugs tha=
t bind to FXR, he
said, could eventually become useful in treating various conditions of the =
small intestine.
Other UT Southwestern researchers involved in the study were Drs. Takeshi I=
nagaki and
Guixiang Zhao, postdoctoral research fellows in molecular biology; Dr. Anto=
nio Moschetta,
postdoctoral research fellow in pharmacology and a research associate in th=
e Howard
Hughes Medical Institute; Youn-Kyoung Lee, student research assistant in mo=
lecular
biology; Li Peng, senior research associate in molecular biology; John Shel=
ton, senior
research scientist in internal medicine; Dr. James Richardson, professor of=
pathology; Dr.
Joyce Repa, assistant professor of physiology; and Dr. David Mangelsdorf, p=
rofessor of
pharmacology and biochemistry and an HHMI investigator. Drs. Ruth Yu and Mi=
chael
Downes of the Salk Institute for Biological Studies in La Jolla, Calif., al=
so participated in the
study.
###
Link to Steven Kliewer's biography: http://www.utsouthwestern.edu/findfac/p=
rofessional/
0,2356,54583,00.html
The work was supported by the National Institutes of Health, the HHMI and T=
he Welch
Foundation.
To automatically receive news releases from UT Southwestern via e-mail, sub=
scribe at
www.utsouthwestern.edu/receivenews
AND
Public release date: 11-Oct-2005
Contact: Aline McKenzie
aline.mckenzie@utsouthwestern.edu
214-648-3404
UT Southwestern Medical Center
Feedback loop found that could forestall liver disease
DALLAS =96 Oct. 11, 2005 =96 Researchers at UT Southwestern Medical Center =
have discovered
that the small intestine communicates with the liver to control the product=
ion of bile acids
=96 a finding that has great medical implications in treating people at ris=
k for certain types of
liver disease.
"We've discovered a new hormone, and new hormones are always exciting," sai=
d Dr. Steven
Kliewer, professor of molecular biology and pharmacology and senior author =
of a study
available online and appearing in the October issue of Cell Metabolism.
The findings may eventually play a role in understanding and preventing liv=
er damage that
can occur in biliary cirrhosis, viral hepatitis, alcoholic liver disease an=
d pregnancy.
The central elements in the research are the body's bile acids =96 powerful=
and essential
detergents that help digest fatty foods and fat-soluble vitamins in the sma=
ll intestine.
The liver makes bile acids out of cholesterol and sends them to the gall bl=
adder, where
they're stored until food is digested. The presence of food stimulates the =
gall bladder into
releasing the bile acids to the small intestine, where they do their work. =
Finally, they're
absorbed into the bloodstream and returned to the liver.
Because they're so powerful, bile acids can damage the body if not controll=
ed properly.
"These bile acids are really nasty in terms of being strong detergents," sa=
id Dr. Kliewer,
holder of the Nancy B. and Jake L. Hamon Distinguished Chair in Basic Cance=
r Research.
Scientists have previously known about a mechanism within the liver that pr=
events too
much bile acid from being produced. Normally, a protein called CYP7A1 stimu=
lates
production of the acids. When enough bile acids are made, they trigger a se=
ries of
reactions that blocks the gene for CYP7A1, and production stops.
For this study, UT Southwestern researchers looked at a protein in mice cal=
led fibroblast
growth factor 15 (FGF15), which is part of a cascade of chemical reactions =
that also dialed
down production of CYP7A1 and reduced the production of bile acids in the l=
iver.
Surprisingly, they found that FGF15 was made in the small intestine, not in=
the liver,
suggesting a new role for the small intestine in regulating bile acid level=
s.
When the researchers injected FGF15 into the bloodstream, CYP7A1 production=
in the liver
was again shut down. Conversely, mutant mice lacking FGF15 made too much CY=
P7A1,
and thus had abnormally high levels of bile acids.
"We can inject FGF15 in the jugular vein, and see the effects in the liver,=
" Dr. Kliewer said.
These discoveries pointed to FGF15 acting as a hormone, which is defined as=
a substance
that's secreted into the bloodstream to work on distant targets.
The findings may be relevant to diseases that involve a condition called ch=
olestatis, in
which the bile ducts are blocked. When that happens bile acids accumulate i=
n the liver and
severe liver disease may follow. Cholestatis can also occur in patients who=
are getting all
their nutrition through intravenous feeding, because the gall bladder never=
receives the
signal from the small intestine to release bile acids.
Dr. Kliewer said perhaps giving cholestatis patients FGF19 =96 the human eq=
uivalent of
FGF15 =96 may turn off the overproduction of harmful bile acids in these ca=
ses.
"So now we have a hormone that's not going to damage the liver, that we cou=
ld perhaps
administer and turn off the production of bile acids, and that could allevi=
ate one of the
important causes of cholestatis," he said. "I think that's one of the excit=
ing implications of
this."
Future research is needed to determine whether the fibroblast growth factor=
protein family
prevents liver disease in animals, Dr. Kliewer said.
Other UT Southwestern researchers involved in the study were Drs. Takeshi I=
nagaki and
Mihwa Choi, postdoctoral research fellows in molecular biology; Dr. Antonio=
Moschetta,
postdoctoral research fellow in pharmacology and a research associate in th=
e Howard
Hughes Medical Institute; Li Peng, senior research assistant in molecular b=
iology; Dr.
Carolyn Cummins, postdoctoral research fellow in pharmacology and HHMI rese=
arch
associate; Dr. Jeffrey McDonald, assistant professor of molecular genetics;=
Dr. James
Richardson, professor of pathology; Dr. Robert Gerard, associate professor =
of internal
medicine and of molecular biology; Dr. Joyce Repa, assistant professor of p=
hysiology; and
Dr. David Mangelsdorf, professor of pharmacology and an HHMI investigator. =
Researchers
from GlaxoSmithKline Research and Development also participated.
The work was supported by the National Institutes of Health, the Welch Foun=
dation and
HHMI.
###
This news release is available on our World Wide Web home page at http://
www8.utsouthwestern.edu/utsw/cda/dept37389/files/248369.html
To automatically receive news releases from UT Southwestern via e-mail, sub=
scribe at
www.utsouthwestern.edu/receivenews
END QUOTES
The blood test results Clover posted indicated anemia.
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