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PubMed2005

Fructose-induced fatty liver disease: hepatic effects of blood pressure and plasma triglyceride reduction.

The most known risk factor for nonalcoholic fatty liver disease (NAFLD) is the metabolic syndrome. In this study, we characterized changes in liver pathology, hepatic lipid composition, and hepatic iron concentration (HIC) occurring in rats given fructose-enriched diet (FED), with and without therapeutic maneuvers to reduce blood pressure and plasma triglycerides. Rats were given FED or standard rat chow for 5 weeks. Rats on FED were divided into 4 groups: receiving amlodipine (15 mg/kg per day), captopril (90 mg/kg per day), bezafibrate (10 mg/kg per day) in the last 2 weeks, or a control group that received FED only. FED rats had hepatic macrovesicular and microvesicular fat deposits develop, with increase in hepatic triglycerides (+198%) and hepatic cholesterol (+89%), but a decrease in hepatic phospholipids (-36%), hypertriglyceridemia (+223%), and hypertension (+15%), without increase in HIC. Amlodipine reduced blood pressure (-18%), plasma triglycerides (-12%), but there was no change in hepatic triglycerides and phospholipids concentrations. Captopril reduced blood pressure (-24%), plasma triglycerides (-36%), hepatic triglycerides (-51%), and hepatic macrovesicular fat (-51%), but increased HIC (+23%), with a borderline increase in hepatic fibrosis. Bezafibrate reduced plasma triglycerides (-49%), hepatic triglycerides (-78%), hepatic macrovesicular fat (-90%), and blood pressure (-11%). We conclude that FED rats can be a suitable model for human NAFLD. Drugs administered to treat various aspects of the metabolic syndrome could have hepatic effects. An increase in HIC in rats with NAFLD could be associated with increased hepatic fibrosis.

Amlodipine↗
PubMed2005

Serum adiponectin, resistin levels and non-alcoholic fatty liver disease in obese children.

The objective is to investigate the relation between the levels of two serum adipocytokines (adiponectin and resistin) and non-alcoholic fatty liver disease (NAFLD) in obese children. In this study, 113 obese children were enrolled and divided into 3 groups. Obese group 1 was defined as obese children without any liver abnormality. Obese group 2 was defined as obese children just with fatty infiltration of the liver in ultrasonic appearance and obese group 3 was defined as obese children with liver function abnormality. The controls consisted of 37 nonobese children without endocrine, metabolic or kidney disease. The levels of serum adiponectin and resistin were measured by ELISA method. Insulin resistance by homeostasis model (HOMA-IR), area under curve of glucose (AUCG), serum total cholesterol, triglyceride, alanine aminotransferase, uric acid, HDL-cholesterol, LDL-cholesterol and body mass index (BMI) were measured as well. In obese children, NAFLD were found in 63 cases (55.75%). Serum adiponectin levels of obese children were significantly lower than that of controls (3.63 vs 5.79 microg/mL, P<0.001) while serum resistin levels were not different (P = 0.876). Moreover, serum adiponectin levels in obese group 1 were significantly higher than that of group 2 and 3 (4.24 vs 3.37 and 3.12 microg/mL, all P<0.05) and no difference was found between obese group 2 and obese group 3 (P>0.05). Serum resistin levels among the three obese groups were 4.37 ng/mL, 3.72 ng/mL and 4.24 ng/mL without significant difference (P = 0.592). NAFLD, BMI, gender and HDL-cholesterol were independent determinants of serum adiponectin levels in children analyzed by multiple regression analysis, which explained 33% of the variance. Serum adiponectin levels were inversely associated with BMI, gender and NAFLD (all P<0.05) and were positively associated with HDL-cholesterol levels (P = 0.033). These results suggest that adiponectin might be a protective factor in NAFLD occurrence in obese children, and that the measurement of adiponectin should be part of the standard evaluation of the obese child and may help to evaluate the occurrence of NAFLD.

Adiponectin↗
PubMed1983

Inhibition of the condensing component of chicken liver fatty acid synthase by iodoacetamide and 5,5'-dithiobis-(2-nitrobenzoic acid).

Chicken liver fatty acid synthase is inhibited by the thiol-modifying reagents 5,5'-dithiobis-(2-nitrobenzoic acid) and iodoacetamide. Total inactivation of the activity for fatty acid synthesis requires the modification of about 8 of the nearly 50 freely accessible thiol groups per molecule. The differential binding of iodo[14C]acetamide to phenylmethylsulphonyl fluoride-modified enzyme in the absence and in the presence of excess acetyl-CoA shows complete modification of one cysteine-SH site of the condensing enzyme and partial modification of the pantetheine-SH site for a total of approx. 1.4 mol of iodoacetamide bound per mol of enzyme. The reaction of the enzyme with 5,5'-dithiobis-(2-nitrobenzoic acid) generates disulphide cross-links for each molecule of the reagent added, but 95% of these cross-links are intrasubunit. Both the iodoacetamide- and 5,5'-dithiobis-(2-nitrobenzoic acid)-modified species catalyse all the component partial reactions of fatty acid synthesis except the condensation reaction. The results obtained with iodoacetamide show that in the dimeric fatty acid synthase modification of one cysteine-SH condensing site and/or one pantetheine-SH site per dimer is sufficient to affect inhibition of condensing activity and the activity for fatty acid synthesis, and are in accord with a recently proposed model for the mechanism of action of animal fatty acid synthases [Kumar (1982) J. Theor. Biol. 95, 263-283].

Acetyl Coenzyme A↗
PubMed1993

[Acute fatty liver of pregnancy: 2 clinical cases].

The clinical evolution and the laboratory pattern of two patients with histopathologically confirmed fatty liver of pregnancy is described. Both babies were delivered vaginally after oxytocic induction and the mothers recovered completely during the puerperium. There was one fetal death in labor secondary to severe abdominal vascular malformation. The other fetus was born healthy.

Acute Disease↗
PubMed2005

The relationship between apoptosis and non-alcoholic fatty liver disease: an evolutionary cornerstone turned pathogenic.

The data currently available favor a model for the pathogenesis of non-alcoholic fatty liver disease that is based on an apparent sequential relationship of intrahepatic apoptosis, inflammation and fibrogenesis. Based on both hepatic and peripheral insulin resistance, the hepatocellular accumulation of triglycerides, termed steatosis, initially leads to an altered metabolism of glucose and free fatty acids in the liver. In response, increased expression of death receptors in simple steatosis enhances the hepatocytes' susceptibility for pro-apoptotic stimuli, thus eliciting excessive hepatocyte apoptosis and inflammation. Evidence indicates that these processes, if prolonged, activate both hepatic stellate and Kupffer cells, thus leading to a vicious circle in which apoptosis, inflammation, cellular activation, and collagen deposition are upregulated even further.

Animals↗
PubMed1992

Carbon-by-carbon discrimination of 13C incorporation into liver fatty acids.

Quantitative carbon-by-carbon analysis would be useful in determining the origin and fate of carbons involved in fatty acid metabolism. Incorporation of 13C from 2-[13C]acetate into specific carbons of liver fatty acids was lowest at the n-2 carbon of saturates and monoenes but was 47% greater at acyl C1 than at C2, suggesting substantial redistribution of the 13C from C2 to C1 of acetyl CoA or malonyl CoA prior to 13C incorporation into fatty acids during de novo synthesis or during elongation. Thus, 13C derived from exogenous acetate can be quantitatively measured and is differentially incorporated into individual carbons depending on position in the fatty acid molecule.

Animals↗
PubMed1993

Effect of prepartum propylene glycol administration on periparturient fatty liver in dairy cows.

Plasma glucose concentration during late gestation was thought to be important for the development of fatty liver near parturition. Thirteen multiparous cows were given a 1-L oral drench of propylene glycol once daily beginning 10 +/- 3.6 d prepartum until parturition. Eleven control cows received a 1-L water drench. Plasma glucose increased following propylene glycol administration. Plasma NEFA concentration was 403 and 234 microM, and plasma insulin concentrations were .354 and .679 ng/ml, for control cows and cows treated with propylene glycol measured from 1 to 7 d prepartum. Plasma NEFA tended to be lower in cows treated with propylene glycol from 1 to 21 d postpartum. Prepartum propylene glycol administration reduced hepatic triglyceride accumulation by 32 and 42% at 1 and 21 d postpartum, respectively. Prepartum plasma BHBA was reduced during propylene glycol administration. Prepartum plasma glucose, NEFA, BHBA, and insulin were strongly correlated with liver triglyceride at 1 d postpartum (r = -.49, .45, .36, and -.49, respectively). Pre- and postpartum DMI were not affected by treatment. Milk production and composition measured through 21 d postpartum were not different between groups.

3-Hydroxybutyric Acid↗
PubMed1987

Binding of acyl-CoA to liver fatty acid binding protein: effect on acyl-CoA synthesis.

The ability of purified rat liver and heart fatty acid binding proteins to bind oleoyl-CoA and modulate acyl-CoA synthesis by microsomal membranes was investigated. Using binding assays employing either Lipidex 1000 or multilamellar liposomes to sequester unbound ligand, rat liver but not rat heart fatty acid binding protein was shown to bind radiolabeled acyl CoA. Binding studies suggest that liver fatty acid binding protein has a single binding site acyl-CoA which is separate from the two binding sites for fatty acids. Experiments were then performed to determine how binding may influence acyl-CoA metabolism by liver microsomes or heart sarcoplasmic reticulum. Using liposomes as fatty acid donors, liver fatty acid binding protein stimulated acyl-CoA production, whereas that from heart did not stimulate production over control values. 14C-labeled fatty acid-fatty acid binding protein complexes were prepared, incubated with membranes, and acyl-CoA synthetase activity was determined. Up to 70% of the fatty acid could be converted to acyl-CoA in the presence of liver fatty acid binding protein but in the presence of heart fatty acid binding protein, only 45% of the fatty acid was converted. Liver but not heart fatty acid binding protein bound the acyl-CoA formed and removed it from the membranes. The amount of product formed was not changed by additional membrane, enzyme cofactors, or incubation time. Additional liver fatty acid binding protein was the only factor found that stimulated product formation. Acyl-CoA hydrolase activity was also shown in the absence of ATP and CoA. These studies suggest that liver fatty acid binding protein can increase the amount of acyl-CoA by binding this ligand, thereby removing it from the membrane and possibly aiding transport within the cell.

Acyl Coenzyme A↗
PubMed2000

Acute fatty liver of pregnancy: diagnosis and management of 8 cases.

OBJECTIVE: To investigate the early recognition and management of acute fatty liver of pregnancy (AFLP) to improve maternal and fetal survival. METHODS: Eight cases of AFLP seen in our hospital during the past three years were studied retrospectively. Symptoms, laboratory findings, timing of liver biopsy, and maternal and fetus outcome were assessed. RESULTS: The mean gestational age at onset was 34 +/- 2 weeks. All cases were primigravida. In the early stages, all patients presented malaise, nausea, vomiting and epigastric distress followed by jaundice in the third trimester of pregnancy. LABORATORY FINDINGS: all had raised transaminases and serum bilirubin (32.5-510.8 mumol/L), hypoalbuminemia (22.4-30.0 g/L), hypofibrinogenemia (< 180 mg/dl), prolonged prothrombin time and prolonged partial thromboplastin time. Maternal complication included hepatic encephalopathy (6 cases), ascites (6), hypoglycemia (5), hematemesis (2), and postpartum hemorrhage (5) and preeclampsia (4). Emergency cesarean section was performed in 3 cases. One mother died of fulminant hepatic failure and the others survived. There was no fetus death. Liver biopsy was done on the 5th to 15th postpartum day in 8 cases. CONCLUSION: With increasing awareness, especially in the early recognition of milder cases, and prompt progressive management including early termination of pregnancy by cesarean section and large dose infusion of fresh frozen plasma and albumin alternately, the prognosis of AFLP can be improved.

Acute Disease↗
PubMed2003

Non-alcoholic fatty liver disease: the problems we are facing.

OBJECTIVE: To review the current state of research in non-alcoholic fatty liver disease (NAFLD). DATA RESOURCES: Searching Medline (1994-2002) and Chinese Medical Journals Index (1998- 2002) for articles on NAFLD. RESULTS: NAFLD is a new and challenging field with increasing recognition although its pathogenesis is poorly understood. "Two hits" hypothesis is still the leading theory guiding current research. CONCLUSIONS: Genetic study is a promising way that might lead to breakthrough in NAFLD research. NAFLD study in China is at an initial stage and there is a long way to go.

China↗
PubMed1976

The involvement of biotin in preventing the fatty liver and kidney syndrome in chicks.

Three experiments were carried out to investigate the involvement of vitamins in the fatty liver and kidney syndrome. The compounds studied, singly and in combination, were thiamin, riboflavin, nicotinic acid, pyridoxine, pantothenic acid, biotin, folic acid vitamin B12, ascorbic acid, choline and inositol and of these, only biotin prevented the syndrome. The minimum levels of supplemental dietary biotin required to prevent mortality varied from 0-05 to 0-15 mg/kg, depending on the diet. These levels were higher than the amounts required for maximum liveweight.

Animal Feed↗
PubMed2006

Glycosylphosphatidylinositol-specific phospholipase d in nonalcoholic Fatty liver disease: a preliminary study.

CONTEXT: Recent studies demonstrated that de novo lipogenesis is increased in patients with nonalcoholic fatty liver disease (NAFLD). Patients with NAFLD also have plasma lipid abnormalities. These lipid abnormalities may in part be related to insulin resistance, which is common in patients with NAFLD. Insulin resistance is associated with alterations in proteins involved in lipid metabolism including glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD), which is involved in triglyceride metabolism. OBJECTIVE: The objective of the study was to determine whether alterations in serum and hepatic levels of GPI-PLD occur in patients with NAFLD. DESIGN AND PATIENTS: We examined the following: 1) levels of serum GPI-PLD in nondiabetics with nonalcoholic steatohepatitis, compared with matched controls; 2) hepatic expression of GPI-PLD mRNA in patients with normal liver or NAFLD; and 3) effect of overexpressing GPI-PLD vs. beta-galactosidase (control) on global gene expression in a human hepatoma cell line. RESULTS: The serum levels of GPI-PLD were significantly higher in patients with nonalcoholic steatohepatitis than in matched controls (119 +/- 24 vs.105 +/- 15 microg/ml, P = 0.047). The hepatic expression of GPI-PLD mRNA was increased nearly 3-fold in NAFLD patients, compared with patients with normal liver (3.1 +/- 2.6 vs. 1.1 +/- 1.0 arbitrary units per microgram total RNA, P = 0.026). Finally, overexpressing GPI-PLD was associated with an increase in de novo lipogenesis genes. CONCLUSIONS: Patients with NAFLD have elevated serum levels and hepatic expression of GPI-PLD, and its overexpression in vitro is associated with increased expression of de novo lipogenesis genes. These results suggest that GPI-PLD may play a role in the pathogenesis of NAFLD and/or its metabolic features and warrants further investigation.

Adult↗
PubMed1999

Acute jaundice in pregnancy: acute fatty liver or acute viral hepatitis?

In this case, the difficulty in differential diagnosis between acute viral hepatitis and acute fatty liver of pregnancy was analyzed. These 2 conditions often raise controversal question regarding the decision making on emergency anesthesia for cesarean section to avert complications and optimize management. The dilemma in which an anesthesiologist is put is whether to promise the anesthesia straightaway in the face of a demonstrable acute jaundice in pregnancy to advise a postponement of surgery until a turn for the better. In this embarrassing situation, the authors suggest that a postpronement of surgery is rational to observe the development during which both the mother and the fetus should be closely monitored. Once the necessity of a cesarean section outweighs the benefit of transitional conservative treatment, it should be performed immediately.

Acute Disease↗
PubMedDate not supplied

Vitamin E-based therapy is effective in ameliorating transaminasemia in nonalcoholic fatty liver disease.

BACKGROUND: Comparative trials of ursodeoxycholic acid (UDCA), vitamin E and weight management programs among patients with nonalcoholic fatty liver disease (NAFLD) are lacking. AIM: To find an effective single agent or combination of agents for management of NAFLD. METHODS: In this retrospective study, consecutive patient with histologically confirmed NAFLD with raised ALT were included. The patients received either weight management (exercise and therapeutic lifestyle changes [TLC] diet with a target to reduce body weight 10% in 6 months) (group I) ; weight management + UDCA (300 mg BID) (group II); or weight management + UDCA + vitamin E (400 mg OD) (group III). Outcome measure was normalization of ALT. RESULTS: 42 patients (18, 12 and 12 in groups I, II and III, respectively) were included between 1996 and 2004. All patients in group III normalized their ALT levels, which was significantly higher than numbers in group I (8/18) and group II (5/12); (p=0.003). Post treatment ALT was significantly lower in group III (28.6 [9.3]) as compared to group I (59.3 [32.2]) and group II (49.0[31.8]); (p=0.01). Type of therapy received was the only factor predictive of ALT normalization. CONCLUSION: Combination regimen containing vitamin E appears to be effective in normalizing ALT among NAFLD patients.

Adolescent↗
PubMed2006

Systemic inflammation in nonalcoholic fatty liver disease is characterized by elevated levels of CCL2.

BACKGROUND/AIMS: To elucidate the role of systemic inflammation in nonalcoholic fatty liver disease (NAFLD). METHODS: Serum samples in 47 patients with histologically verified NAFLD (22 with simple steatosis and 25 with nonalcoholic steatohepatitis [NASH]), and in 30 age-, sex- and ethnicity-matched healthy controls, were assessed for (i) general markers of inflammation (C-reactive protein [CRP], tumor necrosis factor [TNF]-alpha, and interleukin [IL]-6), (ii) chemokines (CC-chemokine ligand [CCL] 2/monocyte chemoattractant protein [MCP]-1, CCL19 and CCL21), (iii) adipocytokines related to insulin resistance and inflammation (adiponectin and leptin) and (iv) a marker of oxidative stress (8-isoprostane-F2alpha). RESULTS: Serum levels of several inflammatory cytokines were increased in NAFLD as compared to controls, and IL-6 (P=0.017), CCL2/MCP-1 (P=0.008) and CCL19 (P=0.001), but not CRP (P=0.199), remained elevated also after correction for sex, body mass index (BMI) and age. Comparing NASH with simple steatosis, levels of TNF-alpha (P=0.024) and CCL2/MCP-1 (P=0.012) were elevated and adiponectin (in women) (P=0.001) were decreased also after adjustment for sex, BMI and presence of the metabolic syndrome. CONCLUSIONS: Our results indicate that patients with NAFLD are characterized by a low-grade systemic inflammation. The high CCL2/MCP-1 levels in NASH might be of importance for the conversion from simple steatosis to NASH.

Adult↗
PubMed2004

Transient remnant removal disease in acute fatty liver of pregnancy.

OBJECTIVE: To elucidate the potential role of an altered lipid metabolism in the pathophysiology of acute fatty liver of pregnancy (AFLP). CASE REPORT: We report on two otherwise healthy women in the 34th gestational week who presented with symptoms of AFLP. Besides characteristic symptoms like nausea, abdominal pain, highly elevated serum amino transferase levels, and increased creatinine concentrations, the patients' clotting system showed consumption and/or decreased synthesis of coagulation factors. Pregnancies were terminated by elective cesarean section because of worsening symptoms. Blood tests normalized quickly and both the mothers and their baby boys could be dismissed in healthy condition. STUDY DESIGN: Blood samples were collected shortly before delivery and 5, 15, 70, and 110 days afterwards. Lipids and apolipoproteins (apo) were analyzed in whole plasma as well as in very low density, intermediate density, low density (LDL), and high density lipoprotein. Total LDL was further separated into 6 LDL subfractions by equilibrium density ultracentrifugation. RESULTS: Before delivery, the LDL subfraction pattern was characterized by the virtual absence of intermediate and most dense LDL. Lipoprotein electrophoresis showed the presence of beta-migrating VLDL. Within days after delivery, the distribution of apoB-containing lipoproteins returned to normal. Genetic variations of apoE, lipoprotein lipases, and the long-chain 3-hydroxyacyl-coenzyme A dehydrogenase were not detected in any of the patients. CONCLUSIONS: The lipoprotein metabolism in the acute phase of AFLP was reminiscent of hepatic lipase deficiency, a disorder characterized by impaired removal of lipoprotein remnants. As these triglyceride-rich particles cause endothelial dysfunction, they may contribute to the pathophysiology of AFLP.

Acute Disease↗