ironjustice

"Methionine and choline-deficient diet-induced steatohepatitis"

Pro-oxidant-mediated hepatic fibrosis and effects of
antioxidant intervention in murine dietary steatohepatitis.
Int J Mol Med. 2009 Aug;24(2):171-80.
Phung N, Pera N, Farrell G, Leclercq I, Hou JY, George J.
Storr Liver Unit, Westmead Millennium Institute,
University of Sydney at Westmead Hospital,
Westmead, NSW 2145, Australia.

The mechanistic significance of oxidative stress to
fibrogenesis in the methionine and choline-deficient
(MCD) diet-induced model of steatohepatitis was
evaluated by antioxidant intervention, using either
vitamin E or L-2-oxothiazolidine-4-carboxylate (OTC),
a cysteine precursor that promotes glutathione synthesis.
Significant depletion of hepatic reduced glutathione (GSH)
and elevation of thiobarbituric acid reactive substances
(TBARS) occurred from week 3 in association with hepatic
injury in mice fed the MCD diet.
Hepatic stellate cell (HSC) activation and increased
collagen alpha1(I) mRNA expression, together with
morphologic fibrosis were evident from week 5.
Vitamin E repleted GSH, reduced TBARS, steatosis,
inflammation, HSC activation and collagen alpha1(I) mRNA
expression, and ameliorated fibrosis.
Vitamin E did not effect the expression of either profibrogenic
cytokines (transforming growth factor-beta 1, connective tissue
growth factor) or matrix remodeling enzymes (tissue inhibitor
of metalloproteinase-1 and -2, matrix metalloproteinase-2 and -13).
Despite repletion of hepatic GSH in OTC-supplemented mice, the
initial benefit in the reduction of hepatic TBARS and inhibition
of collagen alpha1(I) mRNA expression at week 5, failed to protect
these mice from hepatic injury or fibrosis at later time points.
Oxidative stress or products of lipid peroxidation mediate HSC
activation and collagen gene expression directly in the MCD model
of steatohepatitis.
Vitamin E but not glutathione augmentation can interrupt this
pathogenic process.

PMID: 19578790


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

ironjustice

Atheist .. dance ..

"Methionine and choline-deficient diet-induced steatohepatitis"

Pro-oxidant-mediated hepatic fibrosis and effects of
antioxidant intervention in murine dietary steatohepatitis.
Int J Mol Med. 2009 Aug;24(2):171-80.
Phung N, Pera N, Farrell G, Leclercq I, Hou JY, George J.
Storr Liver Unit, Westmead Millennium Institute,
University of Sydney at Westmead Hospital,
Westmead, NSW 2145, Australia.


The mechanistic significance of oxidative stress to
fibrogenesis in the methionine and choline-deficient
(MCD) diet-induced model of steatohepatitis was
evaluated by antioxidant intervention, using either
vitamin E or L-2-oxothiazolidine-4-carboxylate (OTC),
a cysteine precursor that promotes glutathione synthesis.
Significant depletion of hepatic reduced glutathione (GSH)
and elevation of thiobarbituric acid reactive substances
(TBARS) occurred from week 3 in association with hepatic
injury in mice fed the MCD diet.
Hepatic stellate cell (HSC) activation and increased
collagen alpha1(I) mRNA expression, together with
morphologic fibrosis were evident from week 5.
Vitamin E repleted GSH, reduced TBARS, steatosis,
inflammation, HSC activation and collagen alpha1(I) mRNA
expression, and ameliorated fibrosis.
Vitamin E did not effect the expression of either profibrogenic
cytokines (transforming growth factor-beta 1, connective tissue
growth factor) or matrix remodeling enzymes (tissue inhibitor
of metalloproteinase-1 and -2, matrix metalloproteinase-2 and -13).
Despite repletion of hepatic GSH in OTC-supplemented mice, the
initial benefit in the reduction of hepatic TBARS and inhibition
of collagen alpha1(I) mRNA expression at week 5, failed to protect
these mice from hepatic injury or fibrosis at later time points.
Oxidative stress or products of lipid peroxidation mediate HSC
activation and collagen gene expression directly in the MCD model
of steatohepatitis.
Vitamin E but not glutathione augmentation can interrupt this
pathogenic process.


PMID: 19578790


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

I had to laugh when I saw this. You understand about as much of this as
though it were in chinese.

ironjustice

Anyone want to bet those cystic fibrosis patients also have a HIGH
incidence of fatty liver .. ?

Choline-related supplements improve abnormal plasma
methionine-homocysteine metabolites and glutathione
status in children with cystic fibrosis.
Am J Clin Nutr. 2007 Mar;85(3):702-8.
Innis SM, Davidson
AG, Melynk S, James SJ.
Department of Paediatrics, University of British Columbia, Vancouver,
BC, Canada, and the Department of Pediatrics, University of Arkansas
for Medical Sciences, Little Rock, AR.

BACKGROUND: Liver triacylglycerol accumulation and oxidative stress
are common in cystic fibrosis (CF) and also occur in choline
deficiency. Previously, we showed an association between elevated
plasma homocysteine, reduced ratios of S-adenosylmethionine to S-
adenosylhomocysteine (SAM:SAH) and of phosphatidylcholine to
phosphatidylethanolamine, and phospholipid malabsorption in children
with CF. OBJECTIVE: The objective was to address a possible relation
between altered methionine-homocysteine metabolism and choline
metabolism in children with CF. DESIGN: Children with CF were
assigned
without bias to supplementation with 2 g lecithin/d (n = 13), 2 g
choline/d (n = 12), or 3 g betaine/d (n = 10) for 14 d. Plasma
concentrations of methionine, adenosine, cysteine, cysteinyl-glycine,
glutathione, glutathione disulfide (GSSG), and fatty acids; SAM:SAH;
and red blood cell phospholipids were measured within each group of
children with CF before and after supplementation. Plasma from
healthy
children without CF (n = 15) was analyzed to obtain reference data.
RESULTS: Children with CF had higher plasma homocysteine, SAH, and
adenosine and lower methionine, SAM:SAH, and glutathione:GSSG than
did
children without CF. Supplementation with lecithin, choline, or
betaine resulted in a significant increase in plasma methionine, SAM,
SAM:SAH, and glutathione:GSSG and a decrease in SAH (n = 35).
Supplementation with choline or betaine was associated with a
significant decrease in plasma SAH and an increase in SAM:SAH,
methionine, and glutathione:GSSG. Supplementation with lecithin or
choline also increased plasma methionine and SAM. CONCLUSION: We
showed that dietary supplementation with choline-related compounds
improves the low SAM:SAH and glutathione redox balance in children
with CF.


PMID: 17344490 [PubMed - in process] ---------------------------------------------------------------------------****-----
<<snip>>
Lecithin may therefore be the method of choice for accelerating acetylcholine synthesis
<<snip>>


Lancet. 1977 Jul 9;2(8028):68-9. Related Articles, Links


Lecithin consumption raises serum-free-choline levels.


Wurtman RJ, Hirsch MJ, Growdon JH.


Consumption of choline by rats sequentially increases serum-choline,
brain-choline, and brain-acetylcholine concentrations. In man
consumption of choline increases in levels in the serum and
cerebrospinal fluid; its administration is an effective way of
treating


tardive dyskinesia. We found that oral lecithin is considerably more
effective in raising human serum-choline levels than an equivalent
quantity of choline chloride. 30 minutes after ingestion of choline
chloride (2-3 g free base), serum-choline levels rose by 86% and
returned to normal values within 4 hours; 1 hour after lecithin
ingestion, these levels rose by 265% and remained significantly
raised
for 12 hours. Lecithin may therefore be the method of choice for
accelerating acetylcholine synthesis by increasing the availability
of
choline, its precursor in the blood.


PMID: 69151 [PubMed - indexed for MEDLINE]


---------------------------------------------------------------------------****-----


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING http://tinyurl.com/zk9fk

ironjustice

You lose ..

"cystic fibrosis can cause fatty liver"

Best Pract Res Clin Gastroenterol. 2002 Oct;16(5):749-65.
LinksSteatohepatitis in children.
Roberts EA.
Division of Gastroenterology and Nutrition, Room 8267, Black Wing, The
Hospital for Sick Children, 555 University Avenue, Toronto, Ontario,
M5G 1X8, Canada.

Steatohepatitis in children occurs in the childhood version of non-
alcoholic fatty liver disease (NAFLD), as a result of hepatotoxicity
and with certain genetic/metabolic diseases. Until recently, NAFLD was
considered to be rare in children. It is now recognized as an
important childhood liver disease, especially because childhood
obesity is much more common. Children with NAFLD may present as young
as 4 years old; males tend to predominate; fibrosis is often found on
liver biopsy and cirrhosis has been reported. Treatment for childhood
NAFLD currently consists of weight reduction plus regular aerobic
exercise; vitamin E may be an effective adjunctive therapy. Drug
hepatotoxicity and genetic/metabolic diseases that can cause fatty
liver, such as Wilson's disease and cystic fibrosis, must be excluded
since treatment is radically different. Other causes of chronic
hepatitis, such as chronic viral hepatitis, must also be excluded.
Multisystemic inherited diseases with hyperinsulinaemia plus insulin
resistance may have NAFLD as hepatic involvement and should be
identified.

PMID: 12406443


PMID: 19578790


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING http://tinyurl.com/zk9fk

ironjustice

"cystic fibrosis can cause fatty liver"


Best Pract Res Clin Gastroenterol. 2002 Oct;16(5):749-65.
LinksSteatohepatitis in children.
Roberts EA.
Division of Gastroenterology and Nutrition, Room 8267, Black Wing,
The
Hospital for Sick Children, 555 University Avenue, Toronto, Ontario,
M5G 1X8, Canada.


Steatohepatitis in children occurs in the childhood version of non-
alcoholic fatty liver disease (NAFLD), as a result of hepatotoxicity
and with certain genetic/metabolic diseases. Until recently, NAFLD
was
considered to be rare in children. It is now recognized as an
important childhood liver disease, especially because childhood
obesity is much more common. Children with NAFLD may present as young
as 4 years old; males tend to predominate; fibrosis is often found on
liver biopsy and cirrhosis has been reported. Treatment for childhood
NAFLD currently consists of weight reduction plus regular aerobic
exercise; vitamin E may be an effective adjunctive therapy. Drug
hepatotoxicity and genetic/metabolic diseases that can cause fatty
liver, such as Wilson's disease and cystic fibrosis, must be excluded
since treatment is radically different. Other causes of chronic
hepatitis, such as chronic viral hepatitis, must also be excluded.
Multisystemic inherited diseases with hyperinsulinaemia plus insulin
resistance may have NAFLD as hepatic involvement and should be
identified.


PMID: 12406443


PMID: 19578790


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/a3cc3


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

happy oyster

Bets with sub-zeroes are no gread deal.

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happy oyster

Religiotism is a brain disease.

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happy oyster

Better read the bible!

"Toll auch der Trick mit dem Eisen,
um Gottes Macht zu beweisen.
Beileisen ließ Gott nun schwimmen,
um neue Fans zu gewinnen."

http://www.reimbibel.de

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happy oyster

Maniacs are that way.

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