Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two trials were conducted to determine if estrogen contributes to development of fatty liver in dairy cattle. During trial 1, eight late lactation, nonpregnant cows were assigned to 0 or 15 mg estradiol-17 beta benzoate/d treatment. Days 1 to 3 of the trial were for baseline measurements, and treatments were given from d 4 to 21; on d 20 and 21 animals were fasted. Short-term feed deprivation resulted in increased plasma FFA concentrations and rapid accumulation of triglyceride into liver tissue obtained by biopsy. During starvation, plasma FFA concentration and liver triglyceride content were lower for cows receiving the estradiol-17 beta treatment relative to cows receiving control treatment. Very low density lipoprotein concentration in blood increased dramatically in three of four animals during estradiol-17 beta administration. Because of the decrease in milk production during estradiol-17 beta treatment, it was not known whether this represented a decrease in very low density lipoprotein clearance from blood or reflected a lipotropic response to estradiol-17 beta. Therefore, a second trial was conducted employing nonlactating cows, and control and estradiol-17 beta-treated animals were pair fed. The trial was 33 d with d 1 to 3 for baseline measurements, and treatments were administered from d 4 to 33. All animals were starved from d 19 to 23. Estradiol-17 beta increased hepatic lipid and triglyceride accumulation and plasma very low density lipoprotein concentration during starvation. Plasma FFA concentration was also increased by estradiol-17 beta during this time; therefore, a direct or indirect effect of estrogen on hepatic lipid metabolism could not be delineated.
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PMID:Estrogen induction of fatty liver in dairy cattle. 238 18

Estradiol was administered to 3 steers (0.12 mg/kg of body weight/d for 14 consecutive days), followed by 2 days of nonfeeding (starvation). During estradiol administration, liver nuclear estrogen receptor and serum apolipoprotein B-100 (apoB-100), as well as serum triglycerides concentrations were increased, compared with values before administration. Starvation, together with interruption of estradiol administration, resulted in rapid decreases of the receptor, serum apoB-100, and serum triglycerides concentrations, and increase of nonesterified fatty acids concentration. Of the 3 steers, 2 had higher liver triglyceride content, compared with values before treatment. In the control group (3 steers that received vehicle alone, then starved similarly), these concentrations, except for serum nonesterified fatty acids and triglycerides concentrations after starvation, were not changed. In another experiment, serum apoB-100 concentration in dairy cows was significantly (P < 0.05) lower at parturition than values before and after parturition. These results indicate that estradiol may be involved in development of fatty liver in cattle.
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PMID:Effect of estradiol administration and subsequent nonfeeding on liver estrogen receptor, serum apolipoprotein B-100, and serum triglycerides concentrations in steers. 823 36

Hepatitis C virus infections are recognized as a major causative factor of chronic liver disease. A characteristic feature of chronic hepatitis C, alcoholic liver disease and non-alcoholic fatty liver disease is hepatic steatosis. Hepatic steatosis leads to an increase in lipid peroxidation in hepatocytes, which, in turn, activates hepatic stellate cells (HSCs). HSCs are also thought to be the primary target cells for inflammatory and oxidative stimuli, and to produce extracellular matrix components. Based on available clinical information, chronic hepatitis C appears to progress more rapidly in men than in women, and cirrhosis is predominately a disease of men and postmenopausal women. Estradiol is a potent endogenous antioxidant. Hepatic steatosis was reported to become evident in an aromatase-deficient mouse and was diminished in animals after treatment with estradiol. Our previous studies showed that estradiol suppressed hepatic fibrosis in animal models, and attenuated HSC activation by suppressing the generation of reactive oxygen species in primary cultures. Variant estrogen receptors were found to be expressed to a greater extent in male patients with chronic liver disease than in female subjects. A better understanding of the basic mechanisms underlying the gender-associated differences observed in the progression of chronic liver disease would provide valuable information relative to the search for effective antifibrogenic therapies.
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PMID:Protection of estrogens against the progression of chronic liver disease. 1739 11

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.
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PMID:Female hepatology: favorable role of estrogen in chronic liver disease with hepatitis B virus infection. 1770