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PubMed2002

[Clinical characteristics of fatty livers of 61 patients with the insulin resistance syndrome].

OBJECTIVE: To analyse the clinical characteristics of fatty livers of patients with the insulin resistance syndrome. METHODS: With echographic histogram, the acoustic intensity (AV) in six different areas of each fatty liver was measured in 61 patients with the insulin resistance syndrome. The relationship between the average value of AV and some clinical or biochemical parameters were analysed. RESULTS: There were significant differences in AV between the area near the portal venous and the area near the gall bladder, and between males and females as well. AV was positively related to the body mass ratio (BMI), waist circle (W) and hip circle (H); AV was positively related to the waist-hip ratio (WHR) or insulin sensitive index (ISI) in trend; and AV was negatively related to high density lipoprotein cholesterin (HDL-C). CONCLUSION: In patients with the insulin resistance syndrome, fatty density of livers is higher near the portal venous than near the gall bladder. The fatty liver is more serious in females than in males. BMI, W, H and serum HDL-C levels are useful parameters in evaluating the severity of fatty livers.

Adult↗
PubMed1993

Acute fatty liver of pregnancy in a patient with chronic active hepatitis and associated hepatocyte alpha 1-antitrypsin inclusions.

BACKGROUND: Acute fatty liver of pregnancy is a rare, potentially fatal condition that shares many of the signs and symptoms of severe preeclampsia. Early reports of this condition noted alarmingly high fetal and maternal mortality rates. However, recent reports have described more favorable outcomes due to prompt recognition and aggressive treatment. We here describe a patient with acute fatty liver of pregnancy superimposed on chronic active hepatitis. CASE: A 27-year-old woman, para 0-1-2-1, presented at 36 weeks' gestation with a 2-week history of malaise, nausea, emesis, diarrhea, and an 18-lb weight loss. The serum concentrations of transaminase enzymes, bilirubin, and alkaline phosphatase were increased, and a mild coagulopathy was present. The patient underwent repeat cesarean delivery and intraoperative needle biopsy of the liver. Histologic examination of the biopsy demonstrated the characteristic changes of acute fatty liver of pregnancy and chronic active hepatitis with associated alpha 1-antitrypsin hepatocyte inclusions. The serum alpha 1-antitrypsin level was mildly elevated and the phenotype was normal (PiMM), excluding alpha 1-antitrypsin deficiency. Viral and autoimmune etiologies for chronic hepatitis were excluded by laboratory studies. The woman experienced rapid resolution of symptoms and laboratory abnormalities in the immediate postoperative period. CONCLUSION: Acute fatty liver of pregnancy may occur in patients with underlying chronic liver disease. Prompt delivery is necessary to reduce the risk of fetal and maternal mortality.

Acute Disease↗
PubMed2003

The spectrum of fatty liver in obese children and the relationship of serum aminotransferases to severity of steatosis.

OBJECTIVES: Non-alcoholic fatty liver disease is an emerging diagnosis in the pediatric population. Previously, ultrasonography and serum aminotransferases have been used to estimate prevalence of the disorder. A lack of concordance has been noted between these two diagnostic tests. To better understand the spectrum of fatty liver in obese children and the relationship of serum aminotransferases to the severity of steatosis, hepatic MRI was used to quantitate fat content. METHODS: Twenty-two children, ages 6 to 18 years, with obesity (BMI > 95th percentile for age) and hepatomegaly (liver edge more than 2 cm below the right costal margin) underwent hepatic MRI for fat quantitation. Hepatic MRI was performed using a modification of the Dixon method that used a fast gradient echo sequence rather than traditional spin echo. Scan times were sufficiently brief to allow completion within a single breath hold. Serum aminotransferases were obtained within one month of MRI. RESULTS: Twenty-one of 22 subjects had an elevated hepatic fat fraction. Seven of 7 subjects with a fat fraction of < or =18% had a normal serum ALT. Twelve of 13 subjects with fat fraction of >18% had an elevated serum ALT. Hepatic fat fraction correlated with serum ALT but did not correlate with age, BMI, or serum AST. CONCLUSION: The spectrum of fatty liver is larger than detected by screening for abnormal serum aminotransferases alone. Abnormalities in serum ALT occur exclusively in more severe cases of fatty liver.

Adolescent↗
PubMedDate not supplied

The relationship between apolipoprotein E polymorphism, lipoprotein (a) and fatty liver disease.

BACKGROUND/AIMS: The apolipoprotein E (apo E) gene is known to affect plasma lipoprotein-lipid levels, and lipoprotein (a) [Lp(a)] is an atherogenic lipoprotein that is negatively correlated with triglyceride level. The purpose of this study was to investigate the relationship between the apo E genotype, plasma Lp(a) level, and fatty liver. METHODOLOGY: A cross-sectional study was performed on 711 subjects who were diagnosed as having fatty liver by ultrasonography and on 711 sex- and age-matched control subjects. Apo E genotype, plasma Lp(a) concentrations, and serum levels of total cholesterol, triglyceride, LDL-cholesterol, and HDL-cholesterol were measured. RESULTS: Fatty liver subjects were found to have significantly higher triglyceride, and lower HDL-cholesterol levels. According to the multivariate logistic regression analysis, the odds ratios for fatty liver were 2.254 (95% CI 1.697-2.993) for hypertriglyceridemia, 1.841 (95% CI 1.449-2.339) for a high LDL-cholesterol level, 1.509 (95% CI 1.112-2.046) for a low HDL-cholesterol level, and 0.364 (95% CI 0.194-0.684) for a high HDL-cholesterol level. The odds ratios of epsilon4 and a high plasma Lp(a) level for fatty liver were 0.631 (95% CI 0.468-0.850) and 0.607 (95% CI 0.470-0.784) respectively. CONCLUSIONS: Our results suggest that the epsilon4 allele of apo E and plasma Lp(a) concentration may be associated with the pathogenesis of fatty liver.

Adult↗
PubMed1981

Hepatic lipogenesis and mobilization of peripheral fats in the formation of alcoholic fatty liver.

Biochemical mechanisms underlying the development of alcoholic fatty liver was investigated. Acute ethanol (EtOH) administration for 3 days by an inhalation method, and continuous EtOH treatments by feeding with liquid diet or drinking water containing EtOH induced a significant increase of hepatic triglycerides (TG). A small but significant increase of TG was also observed in the blood serum. Although hepatic acetyl CoA carboxylase activity, measured in the presence and absence of citrate, was not altered by either acute or chronic EtOH administrations, fatty acid synthetase and malic enzyme activities in the liver were increased by continuous EtOH administration, but not in the acutely EtOH-treated animals. The incorporations of [14C]palmitate and [14C]acetate into hepatic RG were also increased significantly in animals treated continuously with EtOH. The lipoprotein lipase activity in adipose tissues was activated by both acute and continuous EtOH treatments, whereas lipase activity in adipose tissues and the epinephrine-stimulated and cyclic AMP-mediated release of free fatty acid (FFA) from this tissue were not altered by these treatments. These results indicate that acute alcoholic fatty liver is caused mostly by the increased mobilization of FFA from peripheral adipose tissues via the activation of lipoprotein lipase, whereas alcoholic fatty liver induced by continuous EtOH administration involves the increased synthesis of FFA due to the activation of fatty acid synthetase and malic enzyme in the liver in addition to the increased mobilization of peripheral FFA.

Acetyl-CoA Carboxylase↗
PubMed2003

Impaired insulin-mediated amino acid plasma disappearance in non-alcoholic fatty liver disease: a feature of insulin resistance.

BACKGROUND AND AIM: Insulin resistance is a main feature, and possibly a pathogenic factor, of non-alcoholic fatty liver disease. It is usually measured on glucose metabolism; the effects on amino acid regulation have never been assessed. In particular, no data are available on insulin-dependent branched-chain amino acid metabolism, which is under insulin control. MATERIALS AND METHODS: We measured amino acid disappearance from plasma during an euglycemic glucose clamp in 39 biopsy-proven non-alcoholic fatty liver disease patients and in ten control subjects. A primed-constant infusion of insulin (constant rate, 40 mU/m2 per min for 2 h) was used to raise plasma insulin to approximately 100 mU/l. Euglycemia was maintained by a variable glucose infusion, a measure of tissue insulin sensitivity. Plasma amino acids were assayed during the clamp after ninhidrin derivatization. RESULTS: Fasting plasma amino acids were similar in the two groups. Steady-state insulin levels were significantly higher in non-alcoholic fatty liver disease patients, whereas tissue sensitivity to insulin was reduced by 50%. The plasma disappearance of branched-chain amino acids, as well as the disappearance of the sum of glutamine and glutamate and that of serine were significantly reduced in non-alcoholic fatty liver disease. Differences were maintained after adjustment for steady-state insulin, and correlated with reduced tissue sensitivity to glucose. CONCLUSION: Insulin resistance in non-alcoholic fatty liver disease patients also affects amino acid metabolism, especially for amino acids involved in peripheral muscle nitrogen exchange. The metabolic effects of altered protein/amino acid metabolism must be considered.

Adult↗
PubMed1985

Stoichiometry of substrate binding to rat liver fatty acid synthetase.

Two rat liver fatty acid synthetase preparations, containing 1.6 and 2.0 mol of 4'-phosphopantetheine/mol of synthetase, showed specific activity of 2006 and 2140 nmol of NADPH oxidized/min per mg of protein respectively. The two synthetase preparations could be loaded with either 3.3-4.4 mol of [1-14] acetate or 2.9-3.7 mol of [2-14C]malonate, by incubation with either [1-14C] acetyl-CoA or [2-14C]malonyl-CoA. The 4'-phosphopantetheine site could be more than 90% saturated and the serine site about 80% saturated with malonate derived from malonyl-CoA. However, with acetyl-CoA as substrate, binding at both the 4'-phosphopantetheine and cysteine thiol sites did not reach saturation. We interpret these results to indicate that, whereas the equilibrium constant for transfer of substrates between the serine loading site and the 4'-phosphopantetheine site is close to unity, that for transfer of acetyl moieties between the 4'-phosphopantetheine and cysteine sites favours formation of the 4'-phosphopantetheine thioester. Thus, despite the apparent sub-stoichiometric binding of acetate, the results are consistent with a functionally symmetrical model for the fatty acid synthetase which permits simultaneous substrate binding at two separate active centres.

Acetates↗
PubMed2005

Nonalcoholic fatty liver disease and the metabolic syndrome.

PURPOSE OF REVIEW: Clinical, epidemiological and biochemical data strongly support the concept that nonalcoholic fatty liver disease is the hepatic manifestation of the metabolic syndrome. Insulin resistance is the common factor connecting obesity, diabetes, hypertension and dyslipidemia with fatty liver and the progression of hepatic disease to steatohepatitis, fibrosis, cirrhosis and hepatocellular carcinoma. RECENT FINDINGS: The association of nonalcoholic fatty liver disease with the features of the metabolic syndrome has been confirmed in several epidemiological studies. The diagnostic and clinical significance of raised liver enzymes has been questioned; advanced hepatic disease may also be present in individuals with ultrasonographically detected steatosis and normal aminotransferase levels. The role of adipokines (leptin, adiponectin) and cytokines (tumor necrosis factor-alpha, interleukin-6, transforming growth factor-beta) in disease progression is probably pivotal, mediated by oxidative stress. The importance of iron accumulation in this process has not been confirmed. Treatments aimed at weight loss remain a primary option; among pharmacological interventions, insulin sensitizers (glitazones and metformin) have confirmed beneficial effects on both biochemical and histological data, but new treatments are on the horizon. SUMMARY: Nonalcoholic fatty liver disease prevalence in Western countries is high and there is a trend towards a further increase, with millions of people at risk of advanced liver disease. The epidemiological evidence, the lifestyle origin of the disease and the cost of pharmacotherapy make prevention a primary goal, and will contribute to making behavior therapy the background treatment. We need specific programs and carefully controlled, randomized studies to tackle simultaneously all the components of the metabolic syndrome.

Animals↗
PubMed2005

Lipid peroxidation in bariatric candidates with nonalcoholic fatty liver disease (NAFLD) -- preliminary findings.

BACKGROUND: Pathogenesis of nonalcoholic fatty liver disease (NAFLD) remains incompletely known, and oxidative stress is one of the mechanisms incriminated. The aim of this study was to evaluate the role of liver oxidative stress in NAFLD affecting morbidly obese patients. METHODS: 39 consecutive patients with BMI >40 kg/m2 submitted to Roux-en-Y gastric bypass were enrolled, and wedge liver biopsy was obtained during operation. Oxidative stress was measured by concentration of hydroperoxides (CEOOH) in liver tissue. RESULTS: Female gender was dominant (89.7%) and median age was 43.6 +/- 11.1 years. Histology showed fatty liver in 92.3%, including 43.6% with nonalcoholic steatohepatitis (NASH), 48.7% with isolated steatosis and just 7.7% with normal liver. Liver cirrhosis was present in 11.7% of those with nonalcoholic steatohepatitis. Concentration of CEOOH was increased in the liver of patients with NASH when compared to isolated steatosis and normal liver (0.26+/- 0.17, 0.20+/- 0.01 and 0.14+/- 0.00 nmol/mg protein, respectively) (P < 0.01). Liver biochemical variables were normal in 92.3% of all cases, and no difference between NASH and isolated steatosis could be demonstrated. CONCLUSIONS: 1) Nonalcoholic steatosis, steatohepatitis and cirrhosis were identified in substantial numbers of morbidly obese patients; 2) Concentration of hydroperoxides was increased in steatohepatitis, consistent with a pathogenetic role for oxidative stress in this condition.

Analysis of Variance↗
PubMed2007

Monounsaturated fat decreases hepatic lipid content in non-alcoholic fatty liver disease in rats.

AIM: To evaluate the effects of different types of dietary fats on the hepatic lipid content and oxidative stress parameters in rat liver with experimental non-alcoholic fatty liver disease (NAFLD). METHODS: A total of 32 Sprague-Dawley rats were randomly divided into five groups. The rats in the control group (n = 8) were on chow diet (Group 1), rats (n = 6) on methionine choline-deficient diet (MCDD) (Group 2), rats (n = 6) on MCDD enriched with olive oil (Group 3), rats (n = 6) on MCDD with fish oil (Group 4) and rats (n = 6) on MCDD with butter fat (Group 5). After 2 mo, blood and liver sections were examined for lipids composition and oxidative stress parameters. RESULTS: The liver weight/rat weight ratio increased in all treatment groups as compared with the control group. Severe fatty liver was seen in MCDD + fish oil and in MCDD + butter fat groups, but not in MCDD and MCDD + olive oil groups. The increase in hepatic triglycerides (TG) levels was blunted by 30% in MCDD + olive oil group (0.59 +/- 0.09) compared with MCDD group (0.85 +/- 0.04, P < 0.004), by 37% compared with MCDD + fish oil group (0.95 +/- 0.07, P < 0.001), and by 33% compared with MCDD + butter group (0.09 +/- 0.1, P < 0.01). The increase in serum TG was lowered by 10% in MCDD + olive oil group (0.9 +/- 0.07) compared with MCDD group (1.05 +/- 0.06). Hepatic cholesterol increased by 15-fold in MCDD group [(0.08 +/- 0.02, this increment was blunted by 21% in MCDD + fish oil group (0.09 +/- 0.02)]. In comparison with the control group, ratio of long-chain polyunsaturated fatty acids omega-6/omega-3 increased in MCDD + olive oil, MCDD + fish oil and MCDD + butter fat groups by 345-, 30- and 397-fold, respectively. In comparison to MCDD group (1.58 +/- 0.08), hepatic MDA contents in MCDD + olive oil (3.3 +/- 0.6), MCDD + fish oil (3.0 +/- 0.4), and MCDD + butter group (2.9 +/- 0.36) were increased by 108%, 91% and 87%, respectively (P < 0.004). Hepatic paraoxonase activity decreased significantly in all treatment groups, mostly with MCDD + olive oil group (-68%). CONCLUSION: Olive oil decreases the accumulation of triglyceride in the liver of rats with NAFLD, but does not provide the greatest antioxidant activity.

Animals↗
PubMed1999

Preliminary studies on hepatic carnitine palmitoyltransferase in dairy cattle with or without fatty liver.

The hepatic mitochondrial carnitine palmitoyltransferase (CPT) activity was measured by fluorimetric assay in dairy cows with or without fatty liver. CPT activities in 13 lactating cattle and in 6 non-lactating cows were 304.4+/-86.6 micromol CoA/min per g protein and 169.3+/-84.8 micromol CoA/min per g protein, respectively. This difference was significant (p < 0.05). CPT activities in early lactation (0-110 days after calving), mid-lactation (111-220 days after calving) and late lactation (over 220 days after calving) were 278.9+/-68.0, 312.4+/-124.1 and 320+/-59.3 micromol CoA/min per g protein, respectively. There was no significant difference between the values at different stages of lactation. The CPT activity in 10 lactating cows with fatty liver unrelated to calving was 201.3+/-80.0 micromol CoA/min per g protein. CPT activity in 10 cattle with fatty liver was significantly lower than that in normal lactating cattle. Based on these findings, clinical fatty liver unrelated to calving appears to be associated with a decrease in hepatic CPT activity.

Animals↗
PubMed2005

[Effects of Huatan Xiezhuo Recipe on insulin resistance and leptin in rats with fatty liver].

OBJECTIVE: To observe the effects of Huatan Xiezhuo Recipe (HTXZR) on fatty liver of rats. METHODS: Forty-eight SD rats were randomly divided into five groups: normal control group, untreated group, Dongbao Gantai Tablet (DBGTT)-treated group, low-dose HTXZR-treated group and high-dose HTXZR-treated group. Fatty liver was induced in the rats by hyperlipid diet and intraperitoneal injection of tetracycline. The pathological changes of liver tissues in rats were observed, and the liver function, serum leptin, insulin resistance index, triglyceride (TG) and free fatty acid (FFA) in the liver were detected. RESULTS: The levels of serum leptin, insulin resistance index, FFA and TG in rats of the three treated groups were lower than those of the untreated group (P<0.01), and such effects in the HTXZR-treated groups were more significant than those in the DBGTT-treated group (P<0.05). CONCLUSION: The main action mechanisms of HTXZR in treating fatty liver are probably to promote the lipid metabolism, decrease the leptin and insulin resistance.

Animals↗
PubMed2004

Oval cells compensate for damage and replicative senescence of mature hepatocytes in mice with fatty liver disease.

Hepatic steatosis may have a generally benign prognosis, either because most hepatocytes are not significantly injured or mechanisms to replace damaged hepatocytes are induced. To determine the relative importance of these mechanisms, we compared hepatocyte damage and replication in ethanol-fed and ob/ob mice with very indolent fatty liver disease to that of healthy control mice and PARP-1(-/-) mice with targeted disruption of the DNA repair enzyme, poly(ADP-ribose) polymerase. Compared to the healthy controls, both groups with fatty livers had significantly higher serum alanine aminotransferase values, hepatic mitochondrial H(2)O(2) production, and hepatocyte oxidative DNA damage. A significantly smaller proportion of the hepatocytes from fatty livers entered S phase when cultured with mitogens. Moreover, this replicative senescence was not reversed by treating cultured hepatocytes with agents (i.e., betaine or leptin) that improve liver disease in intact ethanol-fed or leptin-deficient mice. Hepatocytes from PARP1(-/-) mice also had more DNA damage and reduced DNA synthesis in response to mitogens. However, neither mice with fatty livers nor PARP-1-deficient mice had atrophic livers. All of the mice with senescent mature hepatocytes exhibited hepatic accumulation of liver progenitor (oval) cells and oval cell numbers increased with the demand for hepatocyte replacement. Therefore, although hepatic oxidant production and damage are generally increased in fatty livers, expansion of hepatic progenitor cell populations helps to compensate for the increased turnover of damaged mature hepatocytes. In conclusion, these results demonstrate that induction of mechanisms to replace damaged hepatocytes is important for limiting the progression of fatty liver disease.

Animals↗
PubMedDate not supplied

Fatty liver--current look at the old disease.

The report is devoted to the presentation of aetiological factors causing fatty liver, including alcohol, obesity, diabetes mellitus, hyperlipoproteinaemias and drugs. The author discusses morphological changes typical for the fatty liver such as large or small fatty droplets in hepatocytes and rarely coexisting hepatitis (so-called steatohepatitis). The work presents symptoms, changes in biochemical analyses of serum as well as methods of the liver visualisation used in the diagnostics of fatty liver. The treatment in based on the elimination of aetiological factors and properly balanced diet with support of pharmacotherapy in selected cases.

Fatty Liver↗
PubMed2004

Therapeutic potential of interleukin-6 in preventing obesity- and alcohol-associated fatty liver transplant failure.

Donor organ shortage significantly hinders orthotopic liver transplantation therapy, the only effective treatment for chronic end-stage liver disease and acute liver failure. Further complicating this matter is the prevalence of steatosis in 13% to 50% of donor livers obtained from obese and alcoholic individuals. When transplanted, these livers are associated with primary nonfunction and an elevated risk of dysfunction. New therapeutic approaches to render marginal fatty livers worthy for clinical transplantation are actively being sought. Study findings obtained from my group show that in vitro treatment with interleukin-6 (IL-6) dramatically reduces mortality, liver injury, and necrapoptosis in steatotic Zucker rat liver isografts. Findings of additional studies indicate that IL-6 induces hepatoprotection of steatotic liver isografts by preventing sinusoidal endothelial cell damage and, consequently, the amelioration of hepatic microcirculation, and by protecting against hepatocyte death, which is likely mediated through activation of signal transducer and activator of transcription 3/Bcl-x(L). Finally, in vitro IL-6 treatment also prevents mortality associated with alcoholic fatty liver transplants. Relative to the protective effect of IL-6 on steatotic Zucker rat liver, IL-6 is less effective in alcoholic fatty livers, which may be due to the inhibitory effects of ethanol on IL-6 activation of signal transducer and activator of transcription 3 in hepatocytes and sinusoidal endothelial cells. Collectively, these results support the assertion that in vitro IL-6 treatment of steatotic livers may render allografts usable for clinical transplantation, thereby decreasing the gap between the short supply of cadaver liver allografts and high demands for replacement livers. Higher concentrations of IL-6 may be required to protect against alcoholic fatty liver isograft injury because alcohol inhibits IL-6 signaling in the liver.

Animals↗
PubMed1996

Fulminant hepatic failure in pregnant women: acute fatty liver or acute viral hepatitis?

BACKGROUND: Hepatitis E virus, which is endemic in our region, can cause severe liver dysfunction in pregnant women and this can be clinically confused with acute fatty liver of pregnancy. METHODS: We studied the clinical and laboratory data as well as the maternal and fetal outcomes of 12 pregnant women presenting with fulminant hepatic failure in order to determine the etiology of the disease. The clinical diagnoses were subsequently correlated with serologic assays for acute HEV infection. All patients were severely ill with deep jaundice, grade 3-4 encephalopathy and abnormal prothrombin times. RESULTS: A clinical diagnosis of acute viral hepatitis was made in nine patients and of acute fatty liver in the other three cases. IgM and IgG antibodies confirmed acute viral hepatitis E in six of the nine patients while one had acute hepatitis A infection. HEV IgM and IgG antibodies were, however, also positive in two of the three patients thought to have acute fatty liver. Maternal and fetal mortality were 16.6% and 50%, respectively. CONCLUSIONS: We conclude that hepatitis E is the usual cause of acute liver failure in our pregnant women and that clinical and laboratory features do not permit accurate distinction between acute HEV infection and acute fatty liver of pregnancy. The prognosis in patients with acute HEV infection is much better than in other groups with severe liver failure (mortality 16% vs 68%).

Acute Disease↗
PubMed2006

[Effects of acupoint-injection of Kaixilai on TG, TC, MDA, SOD, AST and ALT in the patient of non-alcoholic fatty liver].

OBJECTIVE: To observe therapeutic effect of acupoint-injection of Kaixilai on non-alcoholic fatty liver. METHODS: One hundred cases of non-alcoholic fatty liver were randomly divided into a test group and a control group, 50 cases in each group. The test group were treated with injection of 2 mL Kaixilai injection into Zusanli (ST 36), thrice each week, for 3 months; and the control group were treated with intravenous drip of 200 mL Kaixilai injection, once each day, for 3 months. Changes of triglyceride (TG), total cholesterol (TC), malondialhyde (MDA), superoxide dismutase (SOD), glutamic-oxaloacetic transaminase (AST), glutamic-pyruvic transaminase (ALT), and clinical symptoms were observed in the two groups. RESULTS: There were significant differences before and after treatment in the symptoms, TG, TC, MDA, SOD, AST and ALT in the two groups (P<0.05), with no significant difference between the two groups (P>0.05). CONCLUSION: Acupoint-injection of Kaixilai is an effective therapy for non-alcoholic fatty liver, with convenience, economic and no adverse effect.

Acupuncture Points↗