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At least 19 recordsLinked to original sources
PubMed2003

Activation of hepatic macrophage contributes to hepatic necrosis after post-ischemic reperfusion in alcoholic fatty liver.

Fatty livers are vulnerable to ischemia/reperfusion (I/R) injury. We investigated the role of hepatic macrophages in the I/R injury in the fatty liver. Rats with alcoholic or nonalcoholic fatty liver were subjected to hepatic warm ischemia for 30 min. A bolus of gadolinium chloride (GdCl(3)) was injected intravenously twice before I/R to block hepatic macrophage activity. Alcoholic fatty liver developed more extensive hepatic necrosis with neutrophil infiltration in association with a higher production of cytokine-induced neutrophil chemoattractant (CINC)-1, a potent neutrophil chemokine in rat, after I/R than the nonalcoholic fatty liver or control liver without steatosis. Hepatic apoptosis after I/R increased to a similar degree (3-fold) in each of the two fatty liver models, compared with the control liver. Alcoholic fatty liver exposed to I/R showed a rapid increase in nuclear factor-kappa B (NF-kappaB) binding activity. The GdCl(3) pretreatment significantly reduced NF-kappaB binding activity, CINC-1 level and necrosis in alcoholic fatty liver, despite no significant decrease in the extent of apoptosis. Our results suggest that the activation of hepatic macrophages in alcoholic fatty liver may contribute to hepatic necrosis after I/R, and that the apoptosis might be less dependent on the macrophage activity.

Journal Article↗
PubMed1999

Mitochondrial proteins that regulate apoptosis and necrosis are induced in mouse fatty liver.

Fatty liver is common in nonalcoholic, obese individuals and in lean people who consume alcohol chronically. Although fatty liver is typically benign, a subset of individuals with steatosis develop steatohepatitis and eventually cirrhosis. The disparate outcomes of fatty liver suggest that it reflects a generally beneficial, adaptive response to obesity or alcohol-related stress, but may also increase hepatocyte vulnerability to other challenges. Thus, both protective factors (e.g., Bcl-2 and Bcl-xL) and factors that promote hepatocyte death by apoptosis (e.g., Bax) or necrosis (e.g., UCP2) may be increased in fatty livers. To evaluate this possibility, hepatocyte apoptosis, necrosis, and the expression of factors that regulate cellular viability were assessed in two models of fatty liver (i.e., genetically obese [ob/ob] mice and ethanol [EtOH]-fed lean mice). Findings in mice with fatty livers were compared with lean, control mice that did not have hepatic steatosis. Immunohistochemistry showed striking induction of hepatocyte proteins that promote (e.g., Bax) and inhibit (e.g., Bcl-2 and Bcl-xL) apoptosis in both groups with fatty liver. Both models of fatty liver also increased hepatic transcripts for UCP2, a mitochondrial uncoupling protein, and the protein itself was induced in ob/ob hepatocytes. Despite the up-regulation of factors that threaten cell viability, hepatocyte death was not increased in either ob/ob or EtOH-fed mice, confirming that the liver's protective responses were sufficient under the conditions studied. However, if UCP2 induction reduces the efficiency of adenosine triphosphate (ATP) synthesis, this initially harmless response might enhance the vulnerability of hepatocytes to necrosis.

Animals↗
PubMed1992

[Study of postgastrectomy fatty liver].

Fatty liver was often found concomitantly by the ultrasound during the follow up study of the gastric cancer operation. By ultrasound, development of postgastrectomy fatty liver was seen in 29 out of 176 patients (16.5%) with several gastrectomies. The number of the patients with postgastrectomy fatty liver was 12 out of 104 patients (11.5%) with distal partial gastrectomy with B-I reconstruction, while that was 17 of 72 patients (23.6%) with total gastrectomy with several reconstructions. The incidence of postoperative fatty liver change was significantly higher in the patients under 59 years old compared to the elders. Seventy-five g oral glucose test induced oxyhyperglycemia and hyperinsulinemia in patients with gastrectomy, especially with total gastrectomy. Integrated plasma insulin and triglyceride responses during first one hour in postgastrectomy patients were significantly higher than preoperative values. Moreover, plasma insulin and blood sugar in response to oral glucose test were significantly higher in patients with postgastrectomy fatty liver, compared to those in patients without fatty liver. These results suggested that the postgastrectomy fatty liver was resulted from the abnormality of the glucose metabolism.

Age Factors↗
PubMed1986

Hepatic oestrone sulphotransferase activity and plasma levels of oestrone sulphate, oestrone and oestradiol in male guinea pigs with fatty liver.

Fatty liver was induced in male guinea pigs by combined administration of carbon tetrachloride and azathioprine from the 3rd to 15th week of age. The final body and liver weights were significantly lower than in the control animals, whereas the liver weight in percentage of total body weight was equal. The protein concentration in the 105,000 X g cytosol fraction from the livers was significantly lower than in controls (2P less than 0.02). The oestrone sulphotransferase activity was studied by measuring the oestrone sulphate production when incubating oestrone, PAPS + [35S]PAPS and liver cytosol for 1 h. Significantly less oestrone sulphate per mg protein, per gram liver tissue or total liver was produced with cytosol from animals with fatty liver than from controls (2P less than 0.02). In accordance with decreased oestrone sulphotransferase activity, animals with fatty liver revealed significantly lower plasma levels for oestrone sulphate (2P less than 0.02), whereas the plasma levels for oestrone and oestradiol were increased (2P less than 0.02). The present study supports the assumption of decreased oestrone sulphotransferase activity being important for the changes in plasma oestrogens seen in alcoholic men with fatty liver.

Animals↗
PubMed1995

Hypertriglyceridemia and fatty liver: clinical diagnosis of fatty liver and lipoprotein profiles in hypertriglyceridemic patients with fatty liver.

Fatty liver has prevailed by 14% in the healthy population of this country. The factors contributing genesis of fatty liver were gender (male), obesity, high alcohol consumption, glucose intolerance and hypertriglyceridemia. And hypertriglyceridemia seems to be the common underlying factor to all other causes. The mechanism for accumulation of triglycerides in the liver can be explained at least by increased HTGL activities and elevated apo A-II levels, a postulated co-factor of HTGL. An hypertriglyceridemic patients with fatty liver had the insulin resistance.

Adult↗
PubMed2003

Impairment of hepatic microcirculation in fatty liver.

Fatty liver or hepatic steatosis, which is the result of the abnormal accumulation of triacylglycerol within the cytoplasm of hepatocytes, is a common histological finding in human liver biopsy specimens that is attributed to the effects of alcohol excess, obesity, diabetes, or drugs. There is a general consensus that fatty liver compromises hepatic microcirculation, the common exchange network upon which hepatic arterial and portal inflows converge, regardless of underlying etiology. A significant reduction in hepatic microcirculation has been observed in human fatty donor livers and in experimental models of hepatic steatosis. There is an inverse correlation between the degree of fat infiltration and both total hepatic blood flow and flow in microcirculation. Fatty accumulation in the cytoplasm of the hepatocytes is associated with an increase in the cell volume that reduces the size of the hepatic sinusoid space by 50% compared with a normal liver and may result in partial or complete obstruction of the hepatic sinusoid space. As a result of impaired hepatic microcirculation, the hepatocytes of the fatty liver have reduced tolerance against ischemia-reperfusion injury, which affects about 25% of the donors for liver transplantation because severe steatosis is associated with a high risk of primary nonfunction after liver transplantation.

Animals↗
PubMed2002

Relevance of apolipoproteins in the development of fatty liver and fatty liver-related peripartum diseases in dairy cows.

Most metabolic diseases in dairy cows occur during the peripartum period and are suggested to be derived from fatty liver initially developed during the nonlactating stage. Fatty liver is induced by hepatic uptake of nonesterified fatty acids that are released in excess by adipose tissues attributable to negative energy balance. The fatty accumulation leads to impairment of lipoprotein metabolism in the liver, and the impairment in turn influences other metabolic pathways in extrahepatic tissues such as the steroid hormone production by the corpus luteum. Detailed understanding of the impaired lipoprotein metabolism is crucial for elucidation of the mechanistic bases of the development of fatty liver and fatty liver-related peripartum diseases. This review summarizes results on evaluation of lipoprotein lipid and protein concentrations and enzyme activity in cows with fatty liver and those with ketosis, left displacement of the abomasum, milk fever, downer syndrome and retained placenta. Obtained data strongly suggest that decreases in serum concentrations of apolipoprotein B-100, apolipoprotein A-I and apolipoprotein C-III, a reduction in activity of lecithin:cholesterol acyltransferase and induction of haptoglobin and serum amyloid A are intimately related to the development of fatty liver and fatty liver-related diseases. Moreover, determination of the apolipoprotein concentrations and enzyme activity during the peripartum period is useful for early diagnoses of these diseases.

Abomasum↗
PubMed2002

STAT-3 overexpression and p21 up-regulation accompany impaired regeneration of fatty livers.

Fatty liver is an important cause of morbidity in humans and is linked to impaired liver regeneration after liver injury, but the mechanisms for impaired liver regeneration remain unknown. In the normal liver, the interleukin (IL)-6/STAT-3 pathway is thought to play a central role in regeneration because this pathway is disrupted in IL-6-deficient mice that exhibit impaired liver regeneration after 70% partial hepatectomy (PH). To determine whether inhibition of STAT-3 is involved in fatty liver-related mitoinhibition, regenerative induction of STAT-3 was compared in normal mice and leptin-deficient ob/ob mice that have fatty livers and markedly impaired liver regeneration after PH. In both groups, two waves of STAT-3 activation were observed, the first in endothelia and the second in hepatocytes. Before PH, a significantly higher percentage of ob/ob endothelial and hepatocyte nuclei expressed phosphorylated (activated) STAT-3. After PH, phospho-STAT-3 accumulated in liver nuclei of lean mice and this response was markedly exaggerated in ob/ob mice. Moreover, a striking inverse correlation was noted between hepatocyte nuclear accumulation of phospho-STAT-3 and DNA synthesis (as assessed by bromodeoxyuridine labeling), as well as cyclin D1 mRNA induction and protein expression. In contrast, STAT-3 activation was positively correlated with p21 protein expression in both groups of mice. Because these results link exaggerated STAT-3 activation with impaired hepatocyte proliferation, STAT-3 inhibition cannot be a growth-arrest mechanism in ob/ob fatty livers. Rather, hyperinduction of this factor may promote mitoinhibition by up-regulating mechanisms that impede cell cycle progression.

Animals↗
PubMed2003

Increase of S-100 protein-positive stellate cells in the anterior pituitary of chronic alcoholic patients with fatty liver or fatty cirrhosis.

Healthy subjects 40 years old were used as controls in a study of stellate cells (S-100 protein-containing cells, or S-100 cells) in subjects with chronic alcoholism and fatty liver or fatty cirrhosis. S-100 cells were sparsely found in the adenohypophysis of control subjects, and these cells sometimes formed small clusters. However, in chronic alcoholics with fatty liver or fatty cirrhosis, the number of stellate cells in the anterior pituitary tended to be 17 times higher than it was in the control group. No increase in the number of S-100 positive cells that constitute the large and small follicles in the intermediate pituitary. The physiological function of the S-100 protein has not yet been identified. The fact that an increase in prolactin-secreting and growth hormone-secreting cells, as well as a decrease in gonadotrophs were observed in the hypophysis of alcoholics suggests that the function of stellate cells may be closely related to these phenomena. Our results also imply that the stellate cells found in the anterior and intermediate pituitary differ in function although they both produce S-100 proteins.

Adult↗
PubMedDate not supplied

Experimental observations and clinical implications of fasting and diet supplementation in fatty livers.

Fatty accumulation per se does not appear to affect liver function; however, interest has recently renewed to fatty liver because of the clinical relevance of non alcoholic steato-hepatitis (NASH) and for the increased risk of post-transplant failure in grafted livers with steatosis. Clinical and experimental studies have doubtless demonstrated that oxidative stress ensues in steatotic livers. Mitochondria represent the preferential target of the oxidative injury associated to fatty degeneration and show reduced content of glutathione, higher levels of oxidative products and damages to enzymes involved in the process of ATP synthesis, which become more evident under stressing conditions. Although obese patients with fatty liver are advantaged by weight loss, clinical and experimental observations suggest that fatty livers poorly tolerate excessive food deprivation. These observations represent the rationale for treatment strategies based on the supplementation of antioxidants and energetic substrates rather than solely a diet restriction. This review focuses on data emerging from a series of investigations performed in rats with fatty livers induced by a choline-deficient diet, which resembles human steatosis due to an excessive intake of carbohydrates, and aims to give the cue for the development of therapeutic options able to preserve hepatic function after transplantation of steatotic organs.

Animals↗
PubMed1994

Ultrasonographic hepatic pseudolesions: normal parenchyma mimicking mass lesions in fatty liver.

Fatty hepatic infiltration is usually diffuse but may be patchy or localized. Occasionally, focal areas of normal parenchyma in an otherwise diffuse fatty liver may mimic mass lesions. Typically, these pseudolesions appear as echopoor areas against a background of bright echoes due to fatty infiltration. We report five cases of sonographic pseudolesions with computed tomographic (CT) correlation. Sonographic features that may differentiate these pseudolesions from true abnormalities include their characteristic location in the quadrate lobe, nondisplacement of blood vessels and sometimes their straight-edged appearance of geometric pattern. When these features are present, further investigation is unnecessary. However, patchy foci of normal parenchyma may pose a difficult diagnostic problem which may necessitate computed tomography and biopsy for definitive diagnosis.

Adult↗
PubMed1999

[Disturbances of lipid metabolism and fatty liver].

Fatty liver (FL) is a frequently diagnosed liver disease. There are presented the etiological factors causing FL, including the most frequent alcohol, obesity, diabetes mellitus, hyperlipoproteinemias and drugs. There are discussed some disturbances of lipid metabolism leading to FL. Morphologically we can distinguish FL with large or small fatty droplets. The more severe kind of the disease is FL with hepatitis (steatohepatitis). Symptoms of FL are not characteristic, as well as there are absent typical changes in biochemical analyzes. There are presented methods of the liver visualization (USG, CT) used in the diagnostics of FL. Treatment of FL includes of the elimination of etiological factors first of all, there is still under debate the supportive action of pharmacotherapy in FL.

Fatty Liver↗
PubMed1986

[Immunohistochemical studies on the occurrence of HBs antigen in alcoholic fatty liver and alcoholic fatty liver hepatitis].

120 liver biopsies of alcoholic fatty liver, alcoholic hepatitis and cirrhosis were studied immunohistochemically with regard to the occurrence of HBs-antigen. In no instance HBs-antigen was detected. These findings suggest neither a major influence of hepatitis B-virus on the progression of alcoholic liver cell damage nor a defect in immunologic responsiveness to hepatitis B-virus component in the alcoholic.

Adult↗
PubMed2001

The transcriptional and DNA binding activity of peroxisome proliferator-activated receptor alpha is inhibited by ethanol metabolism. A novel mechanism for the development of ethanol-induced fatty liver.

Fatty acids are ligands for the peroxisome proliferator-activated receptor alpha (PPAR alpha). Fatty acid levels are increased in liver during the metabolism of ethanol and might be expected to activate PPAR alpha. However, ethanol inhibited PPAR alpha activation of a reporter gene in H4IIEC3 hepatoma cells expressing alcohol-metabolizing enzymes but not in CV-1 cells, which lack these enzymes. Ethanol also reduced the ability of the PPAR alpha ligand WY14,643 to activate reporter constructs in the hepatoma cells or cultured rat hepatocytes. This effect of ethanol was abolished by the alcohol dehydrogenase inhibitor 4-methylpyrazole and augmented by the aldehyde dehydrogenase inhibitor cyanamide, indicating that acetaldehyde was responsible for the action of ethanol. PPAR alpha/retinoid X receptor extracted from hepatoma cells exposed to ethanol or acetaldehyde bound poorly to an oligonucleotide containing peroxisome proliferator response elements. This effect was also blocked by 4-methylpyrazole and augmented by cyanamide. Furthermore, in vitro translated PPAR alpha exposed to acetaldehyde failed to bind DNA. Thus, ethanol metabolism blocks transcriptional activation by PPAR alpha, in part due to impairment of its ability to bind DNA. This effect of ethanol may promote the development of alcoholic fatty liver and other hepatic consequences of alcohol abuse.

Acetaldehyde↗
PubMed1975

The visibly fatty liver.

Fatty infiltration of the liver has been identified roentgenographically in several young children. Awareness of this possibility will sometimes allow a radiologist to contribute to the understanding of the patient's metabolic and nutritional state. If a child's liver is shown to be abnormally radiolucent, cystic fibrosis should be considered.

Child, Preschool↗