[On the clinical diagnosis of fatty liver].
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Fatty Liver↗
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[On the etiology and prognosis of fatty liver].
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Fatty Liver↗
[Therapeutic effects of insulin-sensitizing drugs on nonalcoholic fatty liver disease: experiment with rats].
OBJECTIVE: To investigate the therapeutic effects of insulin-sensitizing drugs, rosiglitazone and metformin, on nonalcoholic fatty liver disease (NAFLD). METHODS: Forty-four male SD rats were randomized into 4 groups: normal control group (n = 8, fed with normal food) and NAFLD rats (n = 36, fed with high-fat food). Eight weeks later 4 rats were randomly selected from the NAFLD group and were killed to undergo pathological examination of the liver. When the establishment of experimental model of NAFLD rats was confirmed the remaining 32 NAFLD rats were subdivided into 4 equal subgroups: NAFLD control group (to be fed continuously with high-fat food), rosiglitazone treatment group (fed with normal food and rosiglitazone 1.5 mg x kg(-1) x d(-1) by gastric perfusion), metformin treatment group (fed with normal food and metformin 150 mg x kg(-1) x d(-1) by gastric perfusion), and dietary treatment group (fed with normal food and normal saline by gastric perfusion). By the end of the 12th week, all rats were killed to isolate the samples of serum to test the levels of total cholesterol (TC), triglyceride (TG), alanine transaminase (ALT), aspartate transaminase (AST), and tumor necrosis factor-alpha (TNF-alpha). Samples of liver tissue were taken to undergo pathology to examine fatty degeneration and inflammatory cell infiltration and detection of the levels of TC and TG. In the liver the weights of body and liver were measured so as to calculate the liver index. RESULTS: (1) The levels of serum TC, TG, ALT, and AST, liver TC and TG, and liver index of the NAFLD control group increased significantly, and the liver histology of the NAFLD control group expressed moderate to severe fatty degeneration. (2) The serum TC levels of the rosiglitazone and metformin groups were 2.49 mmol/L +/- 0.68 mmol/L and 2.49 mmol/L +/- 0.58 mmol/L, both significantly lower than that of the NAFLD control group (4.55 mmol/L +/- 1.58 mmol/L, both P < 0.001). The serum TG levels of the rosiglitazone and metformin groups were 0.61 mmol/L +/- 0.17 mmol/L and 0.63 mmol/L +/- 0.16 mmol/L respectively, both significantly lower than that of the NAFLD control group (0.85 mmol/L +/- 0.15 mmol/L, both P < 0.001). The serum level of ALT of the rosiglitazone and metformin groups were 38.3 U/L +/- 10.6 U/L and 43.3 U/L +/- 27.5 U/L respectively, both significantly lower than that of the NAFLD control group (110.6 U/L +/- 44.2 U/L, P < 0.001 and P < 0.05). The serum levels of AST of the rosiglitazone and metformin groups were 141.7 U/L +/- 14.3 U/L and 174.5 U/L +/- 57.9 U/L, both significantly lower than that of the NAFLD control group (251.8 U/L +/- 91.0 U/L, both P < 0.05). The liver TG levels of the rosiglitazone and metformin groups were 18.9 mg/g +/- 2.7 mg/g and 20.4 mg/g +/- 3.6 mg/g respectively, both significantly lower than that of the NAFLD control group (54.8 mg/g +/- 7.6 mg/g, both P < 0.05). The fatty degeneration grades of liver tissues of the rosiglitazone and metformin groups were grade: 0.8 +/- 0.3 and 1.0 +/- 0.2, both significantly lower than that of the NAFLD control group (grade 2.8 +/- 0.5, both P < 0.05). The hepatic inflammation scores of: the rosiglitazone and metformin groups were 0.8 +/- 0.2 and 1.0 +/- 0.3 respectively, both significantly lower than that of the NAFLD control group (1.8 +/- 0.4, both P < 0.05). The levels of abnormality in serum TC and TG, liver TG, and liver histology of the dietary treatment group were all alleviated in comparison with the NAFLD control group, but were somewhat severer than those of the rosiglitazone and metformin treatment groups. (3) The serum TNF-alpha levels of the rosiglitazone and metformin treatment groups were 124.6 pg/mL +/- 21.0 pg/mL, 154.9 pg/mL +/- 32.5 pg/mL respectively, both significantly lower than that of the NAFLD group (324.2 pg/mL +/- 34.2 pg/mL, P < 0.001 and P < 0.05). The liver TNF-alpha levels of the rosiglitazone and metformin treatment groups were 0.24 +/- 0.14 and 0.30 +/- 0.12 respectively, both significantly lower than that of the NAFLD group (0.85 +/- 0.12, both P < 0.001). The levels of FAS mRNA expression of the rosiglitazone and metformin treatment groups were 0.22 +/- 0.14 and 0.29 +/- 0.16 respectively, both significantly lower than that of the NAFLD group (0.68 +/- 0.23, P < 0.001 and P < 0.005). CONCLUSION: The insulin-sensitizing drugs, rosiglitazone and metformin, are effective in the treatment of NAFLD.
Alanine Transaminase↗
Can tetracycline-induced fatty liver in pregnancy be attributed to choline deficiency?
Pregnant women, especially those in their third trimester, are particularly susceptible to tetracycline-induced fatty liver. Experimental evidence obtained in rats suggest that the precipitous fall in maternal liver choline concentration nearing the end of pregnancy could lead to a severe reduction in the lipotropic activity of the liver. It is hypothesised that the liver in this state will be at much greater risk of developing fatty degeneration, especially if it is exposed to hepatotoxic agents such as tetracycline.
Animals↗
Hypertriglyceridemia and fatty liver of fasting rats after administration of emeriamine.
The effect of emeriamine, a potent inhibitor of the entry of fatty acids into mitochondria on lipid metabolism, was examined. Emeriamine (10 mg/kg body weight) was orally administered to rats under the two different physiological conditions of a 2-day fast or refeeding with a high-carbohydrate diet after a 2-day fast. When rats were refed with a high-carbohydrate diet, serum and hepatic ketone bodies and the levels of free fatty acids decreased, and triglycerides significantly increased compared with fasting rats. However, no significant effect of emeriamine on serum and hepatic lipids was observed between two refeeding groups with or without emeriamine. Conversely, when emeriamine was administered to fasting rats, the levels of serum and hepatic triglycerides increased about 11- and 5-fold, respectively. However, the increased level of hepatic triglycerides was not accompanied by the activities of fatty acid synthetase and NADPH-generating enzymes. The analysis of serum lipoprotein revealed that very low-density lipoprotein consisted of triglyceride-rich particles and there were less apolipoproteins in the fasting rat given emeriamine. We also determined the 120-kDA protein content, which was probably dependent on lipogenesis. The level of 120-kDa protein was greatly increased with or without the administration of emeriamine after refeeding with a high-carbohydrate diet, but the concentration of 120-kDa protein was slight in the fasting rat with emeriamine. These results suggest that specific inhibition of fatty acid oxidation by emeriamine diverted the exogenous fatty acid to the esterification pathway, and induced fatty liver and hypertriglyceridemia under fasting conditions.
Animals↗
Inhibitory effect of prolactin on the development of fatty liver induced by ACTH in thrat.
The action and interaction of ACTH and prolactin in the development of fatty liver were investigated in intact rats treated with exogenous hormones. Administration of ACTH or of combinations of ACTH and GH to intact female rats was found to elicit significantly greater increase in liver total lipids content and concentration than administration of combinations of ACTH, or ACTH and GH, with prolactin. In addition, the results support the data reported by Bates et al. (6) that simultaneous application of GH, prolactin and ACTH reduces the effct of ACTH, upon adrenal gland weight.
Adrenal Glands↗
Peroxidation of liver lipids in the pathogenesis of the ethanol-induced fatty liver.
Administration of an acutely intoxicating dose of ethanol produced significant increases in the concentration of liver triglyceride and enhanced the peroxidation of liver lipids in rats. Adipose triglyceride and lipid peroxide concentrations were unaltered. Coenzyme Q(4), an effective antioxidant, significantly inhibited accumulation of liver triglyceride following ethanol intoxication and prevented the peroxidation of liver lipids. These results, which demonstrate the selective ability of ethanol to induce peroxidation of liver lipids, together with the effectiveness of antioxidants, support the previously proposed hypothesis that peroxidation of liver lipids following ethanol intoxication is a factor in the pathogenesis of ethanol-induced liver injury.
Alcoholic Intoxication↗
The binding of lysophospholipids to rat liver fatty acid-binding protein and albumin.
The binding of lysophospholipids to rat liver fatty acid-binding protein (FABP) and to BSA and human serum albumin was investigated by using competitive displacement fluorescence assays by monitoring the displacement of the fluorescent fatty acid probe 11-(dansylamino)undecanoic acid (DAUDA). In addition, direct binding assays using changes in tryptophan fluorescence were possible with albumin. Liver FABP was able to bind a range of lysophospholipids, oleoyl-lysophosphatidic acid (lysoPA), oleoyl-lysophosphatidylcholine (lysoPC), oleoyl-lysophosphatidylethanolamine (lysoPE) and oleoyl-lysophosphatidylglycerol, with similar affinity and a Kd of about 1 microM. Liver FABP was also able to bind lysophospholipids generated by the action of phospholipase A2 or phospholipase A1 (triacylglycerol lipase) on phospholipid vesicles. A possible physiological role for liver FABP in lysophospholipid metabolism within the cell is discussed. Albumin was shown to bind lysoPA with higher affinity than either lysoPC or lysoPE, and the initial minimal DAUDA displacement by lysoPA indicated that lysoPA was binding to the primary high-affinity fatty acid-binding sites on albumin and that, like oleic acid, about 3 mol of ligand/mol was bound to these sites. Kd values in the microM range were indicated for lysoPC and lysoPE, whereas, by comparison with oleic acid, the Kd for lysoPA was significantly lower and high-affinity binding in the nM range was indicated. Overall, the data suggest that, because of structural similarity, lysoPA binds to albumin in a similar manner to long-chain fatty acids.
Animals↗
Hepatic lipids in Reye-Johnson syndrome and in acute encephalopathy without fatty liver.
The relationship between Reye-Johnson syndrome and acute encephalopathy without fatty liver was investigated by comparing the lipid composition of liver samples obtained from five patients with Reye-Johnson syndrome, two patients with acute encephalopathy, and five controls. The mean total hepatic triglyceride concentration was increased nearly sevenfold in Reye-Johnson syndrome and slightly decreased in acute encephalopathy when compared with the mean control value. The mean total hepatic free fatty acid concentration was increased nearly threefold in acute encephalopathy when compared with the mean value in Reye-Johnson syndrome. Total phospholipid content was decreased in the liver in Reye-Johnson syndrome, and this difference was caused mainly by a diminution of the hepatic lecithin fraction. The ratio of palmitic acid to oleic acid and hepatic free fatty acids was 2.5 in Reye-Johnson syndrome, 0.7 in acute encephalopathy, and 0.8 in controls. These results suggest that, despite clinical similarities and laboratory evidence of hepatic dysfunction in both Reye-Johnson syndrome and acute encephalopathy, different pathogenic mechanisms may be responsible for the liver abnormalities found in the two syndromes.
Acute Disease↗
Distribution of reaction intermediates on chicken liver fatty acid synthase.
The distributions of covalent intermediates in the reaction cycle catalyzed by chicken liver fatty acid synthase were studied. In isotope-trapping experiments, 30% of [1-14C] acetyl-enzyme and 6.7% of [2-14C]malonyl-enzyme are converted to long-chain fatty acids, indicating the initiation reaction is partially random. The 3-hydroxybutyryl intermediate is located on the tryptic peptide which contains the 4'-phosphopantetheine (greater than 90%), while the C4-C18 saturated intermediates are distributed both on this peptide and on the peptide that contains the active cysteine. The ratio of intermediates on the two peptides is about unity for chain lengths less than C14, but the amount on the active cysteine progressively decreases for chain lengths of C14, C16, and C18 with trypsinized enzyme. The distributions of carbon chain lengths for the saturated or 3-keto intermediates when acetoacetyl-labeled trypsinized enzyme is incubated with limiting malonyl coenzyme A or NADPH, respectively, show large fractions both of unreacted enzyme and of C16 or longer intermediates. A detailed analysis suggests that the initial condensation and reduction steps are slower than the analogous reactions with longer chain length intermediates. The 3-keto intermediate comprises over 70% of each chain length intermediate detected when NADPH is the limiting substrate, indicating the reduction of the 3-keto intermediates is at least 2 times slower than the reduction of the unsaturated intermediates.
Acetyl Coenzyme A↗
Acute fatty liver of pregnancy. Complication by disseminated intravascular coagulation.
A 31-year-old white woman had idiopathic acute fatty liver of pregnancy. Shortly after admission to the hospital, it became apparent that she was also suffering from disseminated intravascular coagulation. This was treated with heparin sodium, resulting in cessation of overt bleeding and laboratory evidence of moderate abatement of her coagulation abnormalities. Nevertheless, both patient and fetus died. This case report reemphasizes the need for recognition and therapy for the nonhepatic complications of this syndrome.
Acute Disease↗
Anaesthesia for caesarean section in a patient with acute fatty liver of pregnancy.
A 23-yr-old woman presented in labour and hepatic failure. The clinical diagnosis was acute fatty liver of pregnancy. A Caesarean section was performed under epidural anaesthesia, after correction of a coagulopathy. Epidural anaesthesia was chosen because of the potential deleterious effects of general anaesthesia on liver blood flow and function.
Adult↗
Relationships between fatty liver and fertility and some periparturient diseases in commercial Dutch dairy herds.
Declining fertility in dairy cows is frequently suggested to arise from the occurrence of a more negative energy balance and/or the concomitant increased accumulation of triacylglycerol in the liver. Therefore, we performed a field study to assess the clinical effects of postpartum fatty liver in dairy cows on fertility and reproductive disease. Data were collected from 360 cows from nine dairy herds on fertility, diseases, and the liver triacylglycerol content on two occasions during lactation: 6 to 17 days and 38 to 50 days postpartum. The mean concentration of triacylglycerol in the liver was 54.6 mg/g from 6 to 17 days and 38.4 mg/g from 38 to 50 days postpartum. The probability of pregnancy was 30% lower for cows with higher contents of triacylglycerol in the liver compared to the probability for cows with low liver triacylglycerol (P = 0.049). The probability of estrus was also 35% lower for the cows with high triacylglycerol in the liver. This resulted in larger intervals between parturition and first heat and parturition and pregnancy for these cows. There was no effect observed on the first insemination conception rate. Given a certain level of triacylglycerol, recorded milk production had a positive effect on time to pregnancy. The incidences of endometritis, lochiometra and cystic ovarian follicles were not higher in cows with higher liver triacylglycerol contents. Endometritis was associated with a lower first insemination conception rate and more days open (chi2 = 4.26, P = 0.03 and T-test = -2.02, P= 0.04 respectively). We concluded that our results support the idea that differences in the negative energy balance or the accumulation of triacylglycerol in the liver of postpartum dairy cows affect fertility performance. The data also indicate that an increase in milk production has no negative impact on fertility as long as the amount of triacylglycerol in the liver remains the same.
Animals↗
A biochemical explanation for the fatty liver and kidney syndrome of broilers: its alleviation by the short-term use of dietary fat.
1. Fatty livers and kidney syndrome (FLKS) was induced in young broiler chickens by giving them a diet composed principally of wheat and meat meal. 2. FLKS resulted in reduced growth and increased liver weight; fasting for 18 h increased mortality, liver lipid and the specific activity of hepatic ATP-citrate lyase compared with birds fed on a commercial diet. The specific activities of hepatic fructose-1,6-diphosphate-1-phosphohydrolase and pyruvate carboxylase were reduced in birds suffering from FLKS and fasted for 18 h. 3. Feeding of the FLKS-inducing diet supplemented with 150 g animal tallow/kg for 54 h considerably reduced mortality while restoring liver composition and enzyme activities towards those observed in birds fed a commercial diet. Investigations indicated that the glycerol component of the fat was not responsible for the observed responses. 4. The present results suggest that in FLKS insufficiencies of biotin are induced in specific enzyme systems, but the syndrome may be alleviated without the use of supplementary biotin. 5. The evidence indicates that, when stressed, birds affected by FLKS diet from the hypoglycaemia occurring as a result of a reduced capacity for gluconeogenesis.
ATP Citrate (pro-S)-Lyase↗
[Acute fatty liver in pregnancy: a clinicopathologic study].
OBJECTIVE: To investigate the early recognition and management of milder cases of acute fatty liver in pregnancy (AFLP). METHODS: Twelve cases of AFLP treated in our hospital during the past two and half years were retrospectively studied with emphasis on symptoms, laboratory findings, liver biopsy and maternal complications. The 12 cases were classified into 2 groups. Group 1, 6 cases of advanced AFLP diagnosed clinically, were treated in the first year of the study. Group 2, 6 cases of milder AFLP diagnosed by postpartum liver biopsy, were treated during the last one and half years of the study. RESULTS: The mean gestational age at onset was 34 +/- 3 weeks. In the early stage, all cases had malaise, nausea, loss of appetite and epigastric distress followed by jaundice in the third trimester of pregnancy. Laboratory findings included raised transaminases (< or = 300 IU/L) and total serum bilirubin (32.5-510.8 micro mol/L) levels, hypoalbuminemia (18-30 g/L), hypofibrogenemia (< 2.4 g/L), prolonged prothrombin time and prolonged partial thromboplastin time. Maternal complications were frequent including hepatic encephalopathy (9), ascites (9), hypoglycemia (7), renal failure (3), hematemesis (4), preeclampsia (6), and postpartum hemorrhage (5). Cesarean sections were performed in 7 cases. In group 2, both mother and fetuses had 100% survival. However, the mortality of the mothers and fetuses in group 1 were both 50%. CONCLUSIONS: With increasing awareness, especially in the early recognition of AFLP cases and prompt progressive management, including early termination of pregnancy and large dose infusion of fresh frozen plasma, the prognosis of AFLP is obviously improved. Percutaneous liver biopsy should be done when the coagulation tests became normal and the amounts of ascites decreased after delivery.
Acute Disease↗
Nonalcoholic fatty liver disease: assessment of variability in pathologic interpretations.
The exact cause, prevalence, and rate of progression of nonalcoholic fatty liver disease (NAFLD) are unclear because of a lack of agreement on the pathologic features associated with the different types of NAFLD, their clinical syndromes, and because of a lack of accuracy in the interpretation of these pathologic features. Studies of NAFLD would be aided by a consistent and standardized approach to the interpretation of pathologic features. The aim of our study was to assess interobserver and intraobserver variation in the histologic abnormalities associated with NAFLD. We identified histologic features of NAFLD as reported in the literature, and we identified patients with the diagnosis of NAFLD through the databases of two large institutions. Histologic parameters were evaluated for each liver biopsy specimen by four hepatopathologists and twice by two of the four pathologists (blindly). Interobserver and intraobserver concordance among the pathologists was measured by kappa statistics. Nineteen histologic parameters compartmentalized into steatosis, inflammation, liver cell injury, and fibrosis were evaluated on 53 liver biopsy specimens. Significant, substantial, or moderate concordance was present in only six items: the extent of steatosis, sinusoidal location of fibrosis, perivenular fibrosis, grade of fibrosis, ballooning degeneration, and the presence of vacuolated nuclei. Substantial or moderate concordance also was seen for interobserver readings for location of steatosis and periportal injury. Parameters of inflammation were not scored as reliably as parameters of fibrosis and cell injury. We conclude that only some histologic features previously reported in NAFLD (especially those with substantial and moderate concordance for both interobserver and intraobserver interpretation) are interpreted uniformly by experienced pathologists. These histologic features might prove useful for the development of a standardized and reliable pathologic scoring system that includes the full histologic spectrum of NAFLD and its various clinical outcomes.
Biopsy↗
1H NMR spectroscopic studies of lipid extracts from human fatty liver.
Lipid extracts of biopsy samples from normal and non-alcohol-induced fatty human liver were studied by 1H-NMR at 200 MHz. Spectra of the lipid extracts from 10 mg samples were obtained in 6 min with routine acquisition parameters and allowed the calculation of the phosphatidylcholine to total fatty acyl chain ratio, the cholesterol to total fatty acyl chain ratio, the average fatty acyl chain length, the unsaturation ratio and the acylated glycerol to total fatty acyl chain ratio. The data suggest that lipids with a higher ratio of de novo synthesized fatty acyl chains are stored in non-alcohol-induced fatty liver. NMR lipid analysis appears to be a reliable method for the rapid assessment of hepatic lipid composition on bioptic specimens.
Biopsy↗
[An animal model of alcoholic fatty liver and the prevention and treatment with New Qinggan Decoction].
OBJECTIVE: To establish an animal model of alcoholic fatty liver (AFL) and to observe the prevention and treatment with New Qinggan Decoction (NQGD). METHODS: Female SD rats were exposed to the mixture of white spirit and corn oil continuously for up to 6 weeks via an intragastric feeding protocol. The pathologic alteration of the liver and the changes of serum lipid were observed, and the effect of NQGD for preventing and treating AFL was studied. RESULTS: Wide hepatic steatosis was induced in model group rats. Serum triglyceride (TG) and total cholesterol (TC) of the model group were higher than those of the normal group (P<0.01). Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) of the model group were higher than those of the normal group (P<0.05). In NQGD group, hepatic steatosis was milder than that in the model group, and serum TG, TC, AST, ALT descended significantly as compared with the model group (P<0.01). CONCLUSION: AFL model of rats established by feeding the mixture of white spirit and corn oil is similar to the episode of the human AFL, and is easy to intervene with medicine. NQGD can prevent the occurrence of AFL in this model.
Alanine Transaminase↗