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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We previously showed that fatty liver was easily induced in suncus by starvation and that the plasma level of apolipoprotein B (apo B) was very low. There are three possible explanations for the low level of apo B in the animals: low synthetic rate, low secretion rate, and rapid catabolism in the circulation of apo B. We measured post-heparin lipolytic activity (lipoprotein lipase activity), which plays a key role in the catabolism of apo B-containing lipoprotein, VLDL, and found no difference between rats and suncus. We also investigated the hepatic synthetic rate of apo B by liver perfusion studies. Newly synthesized apo B in the suncus liver was detected by immunoprecipitation and found to amount to 12.5% of that in rats. The secretion rate of VLDL in suncus, which was estimated by intravenous injection of Triton WR1339, was 13.8% of that in rats. These two results suggest that there is no major defect in the secretory process. We separated Golgi apparatus from rat and suncus livers, and found much fewer lipoprotein particles in suncus than in rat Golgi apparatus. This evidence suggests that there is no defect in the lipolytic process or hepatic secretory process of apo B-containing lipoprotein, VLDL, but there may be a defect in the assembly process of VLDL and/or in the synthetic process of apo B in suncus. Such a defect may be one of the reasons for starvation-induced fatty liver in suncus.
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PMID:Defect in assembly process of very-low-density lipoprotein in suncus liver: an animal model of fatty liver. 759 40

We have previously reported that fatty liver is easily induced in a novel experimental animal, Suncus murinus (suncus) by withholding food, and that apolipoprotein B (apo B) is not actively synthesized in the liver. In the present paper we describe the effect of starving and refeeding on lipid and lipoprotein metabolism in suncus, in order to explore the mechanisms of induction of fatty liver by starving and of its improvement by refeeding. Starvation induced increase in triglyceride content and decrease in glycogen content of the liver. Although the glycogen content returned to the level before starvation at 12 h after refeeding, the triglyceride content decreased gradually but did not reach the prestarvation level even at 24 h after refeeding in suncus. Plasma lipids, glucose, and insulin levels were decreased by starvation and returned to the levels before starvation between 8 and 24 h after refeeding. On the other hand, the plasma levels of free fatty acid and ketone bodies were elevated significantly by starvation and decreased rapidly by refeeding. These responses to starvation and refeeding, except for the change in hepatic triglyceride, are in common with other experimental animals, suggesting that there are no abnormalities in glucose metabolism or in fatty acid metabolism in suncus. In conclusion, the fatty liver induced by starvation in suncus may be caused by impaired triglyceride transport out of the liver, for which apolipoprotein B is mostly responsible, as reported previously.
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PMID:Effect of starving and refeeding on lipid metabolism in suncus. 820 66

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

The purpose of this study was to determine if the ketone body beta-hydroxybutyrate (beta-HBA) is a useful positive marker for sudden deaths in chronic alcoholics, thought to be due to hypoglycemia. Beta-HBA can be reliably measured in postmortem samples of vitreous humour and urine. In fatalities where there is a history of chronic alcoholism and routine investigations, including autopsy and routine toxicology, yield only a fatty liver as positive findings, a raised level of beta-HBA can be used as an indicator for alcoholic ketosis. Alcoholic ketosis is often associated with antemortem hypoglycemia. Caution should be observed in attributing the significance of ketosis exclusively to alcohol in those conditions where it would otherwise be expected (i.e. diabetic ketoacidosis and chronic starvation). A measurement of this marker of alcoholic ketosis may also help in the investigation of cases where hypothermia or alcohol withdrawal fits are suspected.
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PMID:The investigation of beta-hydroxybutyrate as a marker for sudden death due to hypoglycemia in alcoholics. 830 32

Haptoglobin (Hp), an acute-phase protein, is detected in serum of cows with hepatic lipidosis (fatty liver). To assess the relevance of Hp in fatty liver, induction of Hp was examined, using conditions similar to those involving development of fatty liver in cows. Induction of Hp was achieved by a combination of dexamethasone administration (0.1 mg/kg of body weight) and 2 days' starvation. Haptoglobin appearance in serum was not associated with the increase of alpha 1-acid glycoprotein (a marker for inflammation). This treatment increased serum nonesterified fatty acids concentration and decreased serum triglycerides concentration. Protein kinase C activity was decreased in the cytosolic fractions of liver and mononuclear cells. Reduction of protein kinase C-catalyzed endogenous protein phosphorylation also was observed, particularly in the cytosolic fractions of the tissue and cells. Detection of Hp in serum of cows with fatty liver appears to be explained by the fact that Hp is induced by dexamethasone administration and starvation, which are similar to the condition responsible for fatty liver development. The change of protein kinase C-catalyzed phosphorylation was suggested to be involved in the induction of Hp in cows.
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PMID:Possible involvement of protein kinase C with induction of haptoglobin in cows by treatment with dexamethasone and by starvation. 831 60

We have previously shown that fatty liver was easily induced in suncus by starvation and that the plasma level of apolipoprotein B (apoB) was very low. We also previously reported that a defect in the assembling process of apo B-containing lipoprotein (very low density lipoprotein, VLDL) may be one of the reasons for the low level of plasma apo B and for induction of fatty liver by starvation in suncus. We also found that hepatic acyl coenzyme A cholesterol acyltransferase (ACAT) activity is very low in the animals, resulting in decreased cholesteryl ester contents in the liver. A deficiency of cholesteryl ester in suncus liver may be one of the reasons for the defect in the assembling process of VLDL. In this study, we investigated the effect of cholesterol-feeding, which induces an increase in triglyceride and cholesteryl ester of the liver as a consequence of the induction of both intestinal and hepatic ACAT activities, on the secretion of VLDL. Although the basal ACAT activity of intestinal mucosa was high, cholesterol-feeding did not induce either an increase in plasma lipid or an increase in intestinal ACAT activities in suncus. The hepatic secretion rate of VLDL was estimated by treatment with Triton WR1339, which is well known to inhibit the catabolism of VLDL. Cholesterol-feeding caused a slight increase in hepatic triglyceride and cholesteryl ester but no increase either in the secretion rate of VLDL or in hepatic ACAT activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of acyl coenzyme A cholesterol acyltransferase in intrahepatic processing of apo B-lipoprotein in suncus. 854 56

Hepatic lipidosis occurs when lipid mobilized to the liver exceeds lipid leaving the liver via formation of very-low-density lipoproteins or by oxidation. Hepatic lipidosis in cats is associated with overt liver dysfunction. In affected cats, excess lipid is mobilized to the liver because of starvation. Removal of hepatic lipid may be impaired because of protein malnutrition, a relative carnitine deficiency, or oxidative damage to peroxisomes and other hepatic organelles. Hepatic lipidosis occurs in adult cats, and is manifest by signs of weight loss, depression, vomiting, and icterus. Diagnosis is achieved by evaluating laboratory and diagnostic imaging data, in conjunction with a liver biopsy. Aggressive tube feeding is the treatment of choice. With this treatment, survival rates are 60% to 80%.
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PMID:Feline hepatic lipidosis. 905 87

Systemic carnitine-deficient juvenile visceral steatosis (JVS) mice exhibit decreased expression of some liver-selective genes including those for the urea cycle enzymes during the infantile period. At 25 days, carbamoylphosphate synthetase (CPS) mRNA level was remarkably low in the liver of JVS mice, and the HNF-4 and C/EBP-alpha mRNA contents were also reduced. HNF-3 alpha and C/EBP-beta mRNAs were slightly higher in the liver of JVS mice, and HNF-1 mRNA remained normal. These results, together with the developmental changes of these transcription factor mRNA levels, suggest that HNF-4 and C/EBP-alpha are involved in the suppression of CPS expression. If JVS mice survived the crisis at 4-5 weeks, their body weight caught up with that of control mice around 7 weeks. The steady-state levels of CPS and argininosuccinate synthetase (ASS) mRNAs in the liver of JVS mice were normalized by no later than 8 weeks. Starvation for 48 h caused an increase of about twofold in CPS and ASS mRNA levels in the liver of control mice, while the same treatment failed to increase their levels in the liver of JVS mice. The starvation similarly caused increases in HNF-4 and C/EBP-beta mRNA levels in the liver of both control and JVS mice, but the increases were significantly less in JVS mice than in control mice. Thus, the lack of induction of CPS and ASS mRNAs during development and under starvation in JVS mice correlated with the lower induction of HNF-4 and C/EBP-alpha mRNAs, and of HNF-4 and C/ EBP-beta mRNAs, respectively. Furthermore, all these changes seemed to correlate with the presence of fatty liver and the high serum free fatty acid levels, suggesting that disturbance of fatty acid metabolism affects nitrogen metabolism at least in part via altered gene expression of transcription factors such as HNF-4, C/EBP-alpha, and C/EBP-beta.
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PMID:Suppressed expression of the urea cycle enzyme genes in the liver of carnitine-deficient juvenile visceral steatosis (JVS) mice in infancy and during starvation in adulthood. 905 9

We have previously shown that fatty liver is easily induced in suncus by starvation and that the plasma level of apolipoprotein B (apo B) is very low. We also found that hepatic acyl coenzyme A cholesterol acyltransferase (ACAT) activity is almost absent in the animals, resulting in decreased cholesteryl ester contents in the liver. A deficiency of cholesteryl ester in suncus liver may be one of the reasons for the defect in the assembly process of apo B-containing lipoproteins, leading to a low level of plasma apo B. Another possible explanation for the induction of fatty liver in suncus is a defect in apo B-processing in the liver. In this study, we investigated the hepatic synthetic rate and intrahepatic degradation of apo B using primary cultured hepatocytes derived from suncus and rats. In order to estimate intrahepatic degradation of apo B, we added N-acetylleucyl-leucynorleucinal to the culture medium as an inhibitor of apo B degradation. The basal synthesis of apo B in suncus hepatocytes was 50% of that in rat. Intracellular degradation of apo B was not observed in suncus hepatocytes, while it was obvious in rat hepatocytes. This evidence suggests that the lower secretion rate of apo B lipoprotein is not due to the intrahepatic degradation of apo B, but may be due to the low synthetic rate of apo B.
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PMID:Defect in an intrahepatic degradation of apolipoprotein B in suncus: an animal model of hypobetalipoproteinemia. 950 5

Aflatoxin B1 (AFB1) exerts a chronic carcinogenic and an acute toxic effect on animals. Whereas the mechanism for carcinogenicity is known, no mechanism has been proposed for the toxic action. Among the most prominent signs of aflatoxicosis in several species, including birds and mammals, are hypolipidaemia, hypocholesterolaemia, and hypocarotenaemia, associated with severe hepatic steatosis and weight loss. We suggest that these signs of acute imbalance of lipid metabolism can be the result of the chemical modification (blocking) of key lysyl residues on the LDL protein B-100 by the activated AFB1 molecule. Modified LDLs are not recognised by their specific receptors and thus are rejected by peripheral cells. Upon return to the liver, the modified particles bind to the sinusoidal lining cells. Lipid starvation of peripheral tissues takes place while fat accumulates in the liver. This abnormal state is maintained and reinforced by further modification of nascent apoproteins, which in turn become unable to receive a lipid load for as long as aflatoxin continues to be available in the liver.
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PMID:Aflatoxin B1-induced hepatic steatosis: role of carbonyl compounds and active diols on steatogenesis. 1007 32


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