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PubMed2006

Nonalcoholic fatty liver disease and the metabolic syndrome.

In the last 15 years evidence has been accumulating suggesting that hepatic steatosis may be the starting point for a progressive liver disease. Nonalcoholic steatosis (nonalcoholic fatty liver disease, NAFLD) is now considered a metabolic pathway to advanced liver disease, cirrhosis and hepatocellular carcinoma. Liver disease of other etiology, namely hepatitis C virus, may interact with NAFLD, although the underlying mechanism(s) have not been fully elucidated. Type 2 diabetes mellitus, obesity and dyslipidemia are the principal factors associated with NAFLD, which is now considered the hepatic expression of metabolic syndrome (MS). Several studies have dealt with the relationship of NAFLD and MS, the risk of liver disease associated with the classical features of MS, the importance of insulin resistance as the common soil of different diseases. We still need to clarify the mechanism(s) responsible for liver disease progression from pure fatty liver, to steatohepatitis and to cirrhosis, and the reason(s) why only a few NAFLD cases progress to terminal liver failure while others (the majority) will have a cardiovascular outcome. The epidemics of obesity and diabetes of Western countries is expected to produce a significant increase of metabolic liver disease in the next years. Prevention and intervention programs based on lifestyle are therefore mandatory to reduce the burden of metabolic liver disease.

Fatty Liver↗
PubMed2001

Ultrastructural changes of hepatic stellate cells in the space of Disse in alcoholic fatty liver.

BACKGROUND: Hepatic stellate cell (HSC) has been suggested to play a role in fibrogenesis in alcoholic liver disease. We evaluate the correlation with fibrogenesis and ultrastructure of hepatic stellate cells in alcoholic fatty liver. METHODS: We studied 6 patients with alcoholic fatty liver and 5 non-alcoholic fatty liver. The numbers of fat droplets in hepatic stellate cell was determined by electron microscopy. We also studied the grading of deposition of collagen fibers in the space of Disse. We were to evaluate the structure of hepatic stellate cells in the space of Disse by light and electron microscopy. RESULTS: Wider distribution of fat droplets in hepatic stellate cells in alcoholic fatty liver than in normal liver. The hypertrophied endoplasmic reticulum in hepatic stellate cells is a prominent findings in alcoholic fatty liver. We observed basement membrane-like materials in patients with alcoholic fatty liver with hepatic fibrosis. CONCLUSION: The results demonstrate that, in patients with alcoholic fatty liver by alcoholic liver injury, the hepatic stellate cells may play an important role in the fibrogenesis of perisinusoidal spaces in the liver.

Adult↗
PubMed2000

Alcoholic fatty liver differentially induces a neutrophil-chemokine and hepatic necrosis after ischemia-reperfusion in rat.

Primary graft nonfunction of steatotic liver allograft is one of the factors causing shortage of donor livers. Ischemia/reperfusion (I/R) injury is an important contributory factor to primary graft nonfunction. In this study, we investigated the complex chain of events from transcription factor activation to necrosis through cytokine induction and apoptosis in steatotic rat liver after warm I/R. Rats with alcoholic or nonalcoholic fatty liver were subjected to hepatic warm I/R and compared with control rats. Rats fed an ethanol diet for 6 to 8 weeks developed severe hepatic necrosis accompanied by increased neutrophil recruitment after I/R, compared with rats with nonalcoholic fatty liver or control. Hepatic apoptosis as assessed by DNA fragmentation at 4 hours after I/R, however, increased to a similar degree in each of the 2 fatty liver models compared with the control. Alcoholic fatty liver exposed to I/R showed a rapid increase in nuclear factor-kappaB (NF-kappaB) binding activity at 1 hour after I/R, which preceded an increased expression of tumor necrosis factor alpha (TNF-alpha) and cytokine-induced neutrophil chemoattractant-1 (CINC-1). In contrast, nonalcoholic fatty liver did not show such potentiation of either NF-kappaB activation or cytokine induction after I/R. Our results have indicated that alcoholic fatty liver may differentially induce CINC-1 production and hepatic necrosis after I/R. Furthermore, our results suggest that apoptosis per se does not always lead to necrosis in the liver following I/R.

Animals↗
PubMed2003

The association of fatty liver and diabetes risk.

We examined whether fatty liver, as diagnosed with abdominal ultrasonography, is an independent risk factor for diabetes mellitus during 10 years of follow-up. A total of 840 subjects (467 men and 373 women) were followed for the entire 10 years. The criteria for being non-diabetic were having no history of diabetes, having a fasting plasma glucose level of less than 110 mg/dl and a serum hemoglobin A1c level of 6.4% or less. We indicated that every examine received all examinations after 12 hours of fasting. Well-trained technicians performed abdominal ultrasonography. Although univariate analysis revealed that the presence of fatty liver was related to hyperglycemia 10 years later, multiple logistic regression analysis did not support this finding. In the multiple logistic regression analysis fasting plasma glucose levels at the baseline and age were significantly related to hyperglycemia (odds ratio [OR] = 1.16, 95% confidence interval [CI]: 1.11-1.21, OR = 1.07, 95% CI: 1.01-1.14, respectively). Fatty liver was not an independent risk factor for hyperglycemia in our follow-up study 10 years after the first diagnosis. The high fasting plasma glucose levels were a risk factor for diabetes, even in the normal range.

Adult↗
PubMed1993

[Molecular biology in development of fatty liver--regulation of apolipoprotein B synthesis].

Apolipoprotein B (apo B) synthesis in fatty liver was described in this review. Apo B synthesis has not been intensively studied in fatty liver. Recently, we demonstrated that hepatic apo B mRNA level increased in two experimental models of fatty liver. Davidson et al. reported that apo B mRNA editing was enhanced in fatty liver induced by refeeding after fasting. However, further investigation is needed to clarify whether alteration in apo B gene regulation participates in development of fatty liver.

Animals↗
PubMed1983

[Pathogenesis of endogenous endotoxemia in chronic liver disease--with special reference to the experimental fatty liver in germfree animals].

The effect of intestinal bacterial flora and endotoxin on fatty liver with germfree (GF) and conventional (CV) rat in the 12th and 24th week was investigated after giving fatty diet which was added 1% cholesterol-0.5% cholic acid to the basic diet. Results are as follows. Serum biochemistry Serum GOT, GPT, ALP and cholesterol values increased after giving the fatty diet in both groups. Limulus Gelation Test In CV group, endotoxin was detected in 2 of 10 cases in portal blood and was completely absent in arterial blood. After the fatty diet, endotoxin increased gradually both in portal and arterial blood. Cyclic AMP values on glucagon challenge (P/B ratio) In both groups, the levels of the P/B ratio maintained low values compared with control. In CV group, the values were lower in endotoxin positive cases than negative ones. Hepatic carbohydrate metabolism Abnormal hepatic F6P , glucose, FDP and PEP values were observed in CV group and reduction of the levels of hepatic F6P , G6P and glucose values were remarkable in GF group. Hepatic G6P in CV group and FDP in GF group remained unchanged. Impairment of F6P and G6P in CV group, was significant in endotoxin positive cases than in negative ones.

Animals↗
PubMed1984

Light microscopic and electron microscopic study on morphologic features resulting in the delay of ICG elimination in diabetic and non-diabetic fatty liver.

Disturbances of intravenously administered indocyanin green (ICG) elimination are related to the effective circulating blood volume and the amount of binding protein for transportation in blood plasma through the liver because of the narrowed sinusoidal space due to the enlarged liver cells with fullness of confluent fat droplets in the cytoplasma. However, morphologic changes of the liver resulting in disturbances of ICG elimination could not be actually clarified until the present. Therefore, morphologic changes of the liver resulting in delayed ICG elimination in fatty liver, occurring in diabetes mellitus were investigated in contrast with those in fatty liver in non-diabetic, non-alcoholic diseases of the liver. An electron microscopic study of the liver with delayed ICG elimination revealed thickening and amorphous growth of the sinusoidal wall with obscure pores followed by membraneous formation, narrowness of Disse's space, rarefaction of sinusoidal microvilli and proliferation of collagen fibers, in fatty livers derived from both diabetes mellitus and other diseases. The term "intrasinusoidal block" in fatty liver should be utilized on the basis of these electron microscopic features of the liver.

Adult↗
PubMed2003

The release of insulin in fatty liver.

AIMS: To evaluate the blood levels of lipids, insulin resistance and the release of insulin in the patients with fatty liver. METHODOLOGY: Ninety one patients with fatty liver and forty seven healthy subjects were included in the study. The diagnosis of fatty liver was established by measuring blood levels of lipids and measuring liver echogenity by ultrasound. Fasting plasma levels of lipids, glucose and insulin were measured in the patient group and control group, and the rate of insulin resistance was calculated. HOMA test was used to calculate the insulin resistance. INSULIN RESISTANCE: Fasting insulin value (microU/mL) x Fasting blood glucose value (mmol/L)/22.5 Liver echogenity was measured by a 3.75 mHz ultrasound probe and was graded by comparison with renal cortical paranchymal echogenity in both groups. Increased blood levels of lipids and increased liver echogenity on the ultrasonography were accepted as fatty liver. Liver biopsy was not applied. The patients with liver and/or renal paranchymal disease were excluded from the study. The rate of release of insulin was calculated according to the following formula. 20 x plasma levels of insulin (mIU/mL)/plasma levels of glucose (mmol/L)-3.5 RESULTS: In the fatty liver group, plasma levels of cholesterol were 253.5 +/- 41.0 (161-440) mg/dL, plasma levels of triglycerides were 231.8 +/- 74.4 (45-493) mg/dL, grading of liver echogenity was 1.9 +/- 0.6 (1-3), the rate of release of insulin was 111.5 +/- 82.2 (3-463.8) and the rate of insulin resistance was 22.4 +/- 4.1 (18.3-26.5). In the control group, plasma levels of cholesterol were 173.4 +/- 19.1 (122-207) mg/dL, plasma levels of triglycerides were 110.5 +/- 39.3 (40-185) mg/dL, grading of liver echogenity was 1.0 +/- 0.1 (1-1), the rate of release of insulin was 129.6 +/- 84.1 (14.5-360) and the rate of insulin resistance was 20.3 +/- 2.1 (18.2-22.4). The rate of release of insulin and insulin resistance were similar in both groups (p>0.5). CONCLUSIONS: We observed that the rate of release of insulin in the patients with fatty liver was not different from that of the healthy subjects.

Case-Control Studies↗
PubMedDate not supplied

Prognosis of patients with a diagnosis of fatty liver--a registry-based cohort study.

BACKGROUND/AIMS: There are very limited data available regarding the prognosis of patients with fatty liver. We examined the overall and cause-specific mortality of fatty liver patients in a large Danish cohort. METHODOLOGY: In the Danish National Registry of Patients, we identified 7,372 patients discharged with a diagnosis of fatty liver from a Danish hospital between 1977 and 1993. Causes of death were identified in the Danish Death Registry. We estimated the standardized mortality ratio by comparing with the general population. RESULTS: Most patients (76%) had alcoholic fatty liver. During follow-up, 2,914 (40%) died. The commonest cause of death was hepatobiliary disease (25% of deaths). Mortality was increased 5.4-fold (95% CI 5.2-5.6) in patients with alcoholic fatty liver, and 2.6-fold (95% CI 2.4-2.9) in patients with non-alcoholic or unspecified fatty liver. Overall, in the first year of follow-up, mortality was increased more than 7-fold, almost 5-fold in the second to fifth years, and more than 3-fold after that. Mortality was similar among genders and among diabetics and non-diabetics, and remained increased after censoring patients upon diagnosis of liver cirrhosis. CONCLUSIONS: The mortality of patients with a hospital discharge diagnosis of fatty liver was higher than that of the general population.

Cause of Death↗
PubMed2006

Acute fatty liver of pregnancy.

Acute fatty liver of pregnancy (AFLP) is a rare, potentially fatal complication that occurs in the third trimester or early postpartum period. Although the exact pathogenesis is unknown, this disease has been linked to an abnormality in fetal fatty acid metabolism. Early diagnosis of AFLP sometimes can be difficult because it shares features with other common conditions such as pre-eclampsia, viral hepatitis and cholestasis of pregnancy. However, a careful history and physical examination, in conjunction with compatible laboratory and imaging results, are often sufficient to make the diagnosis, and liver biopsy is rarely indicated. Supportive care and expeditious delivery are essential to optimal maternal-fetal outcomes and remain as the mainstay treatment for AFLP.

Acute Disease↗
PubMed2006

Associations between serum 25-hydroxyvitamin D3 concentrations and liver histology in patients with non-alcoholic fatty liver disease.

BACKGROUND AND AIM: To explore associations between serum 25-hydroxyvitamin D(3) [25(OH)D] concentrations and liver histology in patients with non-alcoholic fatty liver disease (NAFLD). METHODS AND RESULTS: We studied 60 consecutive patients with biopsy-proven NAFLD, and 60 healthy controls of comparable age, sex and body mass index (BMI). NAFLD patients had a marked decrease in winter serum 25(OH)D concentrations (51.0+/-22 vs. 74.5+/-15 nmol/L, P<0.001) compared with controls. Metabolic syndrome (MetS; as defined by the Adult Treatment Panel III criteria) and its individual components occurred more frequently among NAFLD patients. The marked differences in 25(OH)D concentrations observed between the groups were little affected by adjustment for age, sex, BMI, creatinine, calcium, homeostasis model assessment (HOMA)-insulin resistance, and the presence of the MetS. Interestingly, among NAFLD patients, decreased 25(OH)D concentrations were closely associated with the histological severity of hepatic steatosis, necroinflammation and fibrosis (P<0.001 for all) independent of age, sex, BMI, creatinine, calcium, HOMA-insulin resistance, and presence of the MetS. CONCLUSIONS: Compared with controls, NAFLD patients have a marked decrease in serum 25(OH)D concentrations, which is closely associated with histopathological features of NAFLD. Further investigation into whether vitamin D(3) may play a role in the development and progression of NAFLD appears to be warranted.

Biomarkers↗
PubMed2003

Increase in the prevalence of fatty liver in Japan over the past 12 years: analysis of clinical background.

BACKGROUND: The aim of this investigation was to elucidate the time-course of changes in the prevalence of fatty liver, and to analyze its clinical backgrounds over the previous 12-year period. METHODS: Thirty-nine thousand one hundred and fifty-one individuals who visited the Tokai University Hospital Health Checkup Center from 1989 to 2000 were examined for the presence of fatty liver, and their clinical backgrounds were analyzed. RESULTS: In 1989, the prevalence of fatty liver was 12.6%, and it rose gradually thereafter, reaching 30.3% in 1998, corresponding to a 2.4-fold increase over the prevalence rate in 1989. The average prevalence was about twice as high in males (26.0%) as in females (12.7%). The prevalence was uniformly high in males in all ages, while the prevalence in females tended to rise gradually with age. Body mass index (BMI) was found to be the variable most closely related to the onset of fatty liver. On the other hand, nonobese individuals with a BMI of less than 25 kg/m(2) accounted for approximately half of all the patients with fatty liver, and this proportion remained almost unchanged during the 12-year survey period. It was therefore difficult to simply attribute the increase in the prevalence of fatty liver to the increased prevalence of obesity. In the 35 519 repeat examinees (repeaters), it was found that 5088 individuals (14.3%) developed fatty liver, and fatty liver resolved in 1248 individuals (3.5%). As fatty liver developed, the BMI increased by 1.0 +/- 1.3 kg/m(2). As fatty liver disappeared, the BMI decreased by 1.0 +/- 1.5 kg/m(2). CONCLUSIONS: These results suggest that the absolute value of the BMI, as well as the relative changes in the BMI in each individual, may be related to the onset of fatty liver. The aim of this investigation was to elucidate the time-course of changes in the prevalence of fatty liver, and to analyze its clinical backgrounds over the previous 12-year period.

Adult↗
PubMed1999

Nature of o-phthalaldehyde reaction with pigeon liver fatty acid synthetase.

Pigeon liver fatty acid synthetase (FAS) was inactivated irreversibly by stoichiometric concentration of o-phthalaldehyde exhibiting a bimolecular kinetic process. FAS-o-phthalaldehyde adduct gave a characteristic absorption maxima at 337 nm. Moreover this derivative showed fluorescence emission maxima at 412 nm when excited at 337 nm. These results were consistent with isoindole ring formation in which the -SH group of cysteine and epsilon-NH2 group of lysine participate in the reaction. The inactivation is caused by the reaction of the phosphopantetheine -SH group since it is protected by either acetyl- or malonyl-CoA. The enzyme incubated with iodoacetamide followed by o-phthalaldehyde showed no change in fluorescence intensity but decrease in intensity was found in the treatment of 2,4,6-trinitrobenzenesulphonic acid (TNBS), a lysine specific reagent with the enzyme prior to o-phthalaldehyde addition. As o-phthalaldehyde did not inhibit enoyl-CoA reductase activity, so nonessential lysine is involved in the o-phthalaldehyde reaction. Double inhibition experiments showed that 5,5'-dithiobis-(2-nitrobenzoic acid) (DTNB), a thiol specific reagent, binds to the same cysteine which is also involved in the o-phthalaldehyde reaction. Stoichiometric results indicated that 2 moles of o-phthalaldehyde were incorporated per mole of enzyme molecule upon complete inactivation.

Animals↗
PubMed1986

Serum cholinesterase in patients with fatty liver.

In search of a practical biochemical test that will reflect hepatic steatosis, we assessed the significance of serum cholinesterase activity in 48 patients with nonalcoholic fatty liver, 16 obese subjects without fatty liver, 30 cases of chronic persistent hepatitis, 38 cases of chronic active hepatitis, and 20 cases of liver cirrhosis. Increased cholinesterase activity was observed in nonobese as well as obese patients with fatty liver, whereas obese subjects without fatty liver showed levels in the upper normal range. When we set a cutoff level above the upper normal limit, half of the patients with fatty liver showed values above it, with only a few overlaps with other patients. When obese patients with fatty liver took a low-caloric diet, cholinesterase activity decreased, clearly reflecting improvement of hepatic steatosis. Thus, measurement of cholinesterase activity is of diagnostic value and an alternative to computed tomography in hepatic steatosis, and will provide a practical measure for the assessment of effects during follow-up.

Cholinesterases↗
PubMed2004

Liver-specific deletion of negative regulator Pten results in fatty liver and insulin hypersensitivity [corrected].

In the liver, insulin controls both lipid and glucose metabolism through its cell surface receptor and intracellular mediators such as phosphatidylinositol 3-kinase and serine-threonine kinase AKT. The insulin signaling pathway is further modulated by protein tyrosine phosphatase or lipid phosphatase. Here, we investigated the function of phosphatase and tension homologue deleted on chromosome 10 (PTEN), a negative regulator of the phosphatidylinositol 3-kinase/AKT pathway, by targeted deletion of Pten in murine liver. Deletion of Pten in the liver resulted in increased fatty acid synthesis, accompanied by hepatomegaly and fatty liver phenotype. Interestingly, Pten liver-specific deletion causes enhanced liver insulin action with improved systemic glucose tolerance. Thus, deletion of Pten in the liver may provide a valuable model that permits the study of the metabolic actions of insulin signaling in the liver, and PTEN may be a promising target for therapeutic intervention for type 2 diabetes.

Adipose Tissue↗
PubMed2006

Non-alcoholic fatty liver disease in obese children evaluated by magnetic resonance imaging.

AIM: To investigate the prevalence of non-alcoholic fatty liver disease (NAFLD) in a group of obese children (BMI > 97th %) and to establish correlations between the severity of hepatic fatty infiltration, auxological findings and parameters of insulin resistance. METHODS: 44 obese children, aged 6-16 years, with a BMI above the 97th centile were selected for analysis. Hepatic fat content was assessed by phase contrast MRI. Demographic data included weight, height, body mass index, body fat mass and waist circumference. Blood tests included fasting blood glucose, fasting insulin and lipid profile. Insulin sensitivity was evaluated with QUICKI. RESULTS: Elevated hepatic fat fraction (FF) was identified in 14 subjects (31.8%; 0.07 SEM). Children with fatty liver (FF > 9%) had higher ALT (P<0.0001), AST (P=0.002) and triglycerides (P=0.008) values compared to the children without NAFLD. All the children showed a decreased insulin sensitivity (P<0.0001), but no difference was found between children with or without NAFLD. The degree of liver fatty infiltration was positively correlated with ALT (P<0.0001), AST (P<0.002) and gammaGT (P<0.0001), with height (P<0.006) and BMI (P<0.05) but not with estimates of body fat mass or fat distribution. CONCLUSION: Obese children are frequently affected by NAFLD, which cannot be predicted by clinical and/or anthropometrical findings. There is however a strict correlation between the degree of liver fatty infiltration and elevation of liver enzymes.

Adolescent↗