Add group to favorites
Back to post list
Send new message to group Search:
Post Subject:
Estrogen and Liver Disease
Estrogen and Liver Disease
Since estrogen lowers red blood cell count .. could .. THIS
theoretical intervention be just another form of .. bloodletting .. ?
World J Gastroenterol. 2007 Aug 28;13(32):4295-305.
Female hepatology: Favorable role of estrogen in chronic liver disease
with hepatitis B virus infection.
Shimizu I, Kohno N, Tamaki K, Shono M, Huang HW, He JH, Yao DF.
Department of Digestive and Cardiovascular Medicine, Institute of
Health Biosciences, University of Tokushima Graduate School, 3-18-15
Kuramoto-cho, Tokushima 770-8503, Japan. shimizui@clin.med.tokushima-
u.ac.jp.
Chronic hepatitis B virus (HBV) infection is the most common cause of
hepatic fibrosis and hepatocellular carcinoma (HCC), mainly as a
result of chronic necroinflammatory liver disease. A characteristic
feature of chronic hepatitis B infection, alcoholic liver disease and
nonalcoholic fatty liver disease (NAFLD) is hepatic steatosis. Hepatic
steatosis leads to an increase in lipid peroxidation in hepatocytes,
which, in turn, activates hepatic stellate cells (HSCs). HSCs are the
primary target cells for inflammatory and oxidative stimuli, and these
cells produce extracellular matrix components. Chronic hepatitis B
appears to progress more rapidly in males than in females, and NAFLD,
cirrhosis and HCC are predominately diseases that tend to occur in men
and postmenopausal women. Premenopausal women have lower hepatic iron
stores and a decreased production of proinflammatory cytokines.
Hepatic steatosis has been observed in aromatase-deficient mice, and
has been shown to decrease in animals after estradiol treatment.
Estradiol is a potent endogenous antioxidant which suppresses hepatic
fibrosis in animal models, and attenuates induction of redox sensitive
transcription factors, hepatocyte apoptosis and HSC activation by
inhibiting a generation of reactive oxygen species in primary
cultures. Variant estrogen receptors are expressed to a greater extent
in male patients with chronic liver disease than in females. These
lines of evidence suggest that the greater progression of hepatic
fibrosis and HCC in men and postmenopausal women may be due, at least
in part, to lower production of estradiol and a reduced response to
the action of estradiol. A better understanding of the basic
mechanisms underlying the sex-associated differences in hepatic
fibrogenesis and carciogenesis may open up new avenues for the
prevention and treatment of chronic liver disease.
PMID: 17708600 [PubMed - in process]
Who loves ya.
Tom
Jesus Was A Vegetarian!
* jesuswasavegetarian.7h . com
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
Since estrogen lowers red blood cell count .. could .. THIS
theoretical intervention be just another form of .. bloodletting .. ?
World J Gastroenterol. 2007 Aug 28;13(32):4295-305.
Female hepatology: Favorable role of estrogen in chronic liver disease
with hepatitis B virus infection.
Shimizu I, Kohno N, Tamaki K, Shono M, Huang HW, He JH, Yao DF.
Department of Digestive and Cardiovascular Medicine, Institute of
Health Biosciences, University of Tokushima Graduate School, 3-18-15
Kuramoto-cho, Tokushima 770-8503, Japan. shimizui@clin.med.tokushima-
u.ac.jp.
Chronic hepatitis B virus (HBV) infection is the most common cause of
hepatic fibrosis and hepatocellular carcinoma (HCC), mainly as a
result of chronic necroinflammatory liver disease. A characteristic
feature of chronic hepatitis B infection, alcoholic liver disease and
nonalcoholic fatty liver disease (NAFLD) is hepatic steatosis. Hepatic
steatosis leads to an increase in lipid peroxidation in hepatocytes,
which, in turn, activates hepatic stellate cells (HSCs). HSCs are the
primary target cells for inflammatory and oxidative stimuli, and these
cells produce extracellular matrix components. Chronic hepatitis B
appears to progress more rapidly in males than in females, and NAFLD,
cirrhosis and HCC are predominately diseases that tend to occur in men
and postmenopausal women. Premenopausal women have lower hepatic iron
stores and a decreased production of proinflammatory cytokines.
Hepatic steatosis has been observed in aromatase-deficient mice, and
has been shown to decrease in animals after estradiol treatment.
Estradiol is a potent endogenous antioxidant which suppresses hepatic
fibrosis in animal models, and attenuates induction of redox sensitive
transcription factors, hepatocyte apoptosis and HSC activation by
inhibiting a generation of reactive oxygen species in primary
cultures. Variant estrogen receptors are expressed to a greater extent
in male patients with chronic liver disease than in females. These
lines of evidence suggest that the greater progression of hepatic
fibrosis and HCC in men and postmenopausal women may be due, at least
in part, to lower production of estradiol and a reduced response to
the action of estradiol. A better understanding of the basic
mechanisms underlying the sex-associated differences in hepatic
fibrogenesis and carciogenesis may open up new avenues for the
prevention and treatment of chronic liver disease.
PMID: 17708600 [PubMed - in process]
Who loves ya.
Tom
Jesus Was A Vegetarian!
* jesuswasavegetarian.7h . com
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
Next: Study shows link between alcohol consumption and hiv disease progression
Previous: Reducing Iron Overload
