[Biochemical analysis of liver lipids in fatty liver].
Explore the source record for details and available documents.
Alcoholism↗
SEARCH · Search PubMed
Results for “FATTY LIVER”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Discriminant analysis of ultrasonic texture data in diffuse alcoholic liver disease. 1. Fatty liver and cirrhosis.
Explore the source record for details and available documents.
Analysis of Variance↗
Defect in assembly process of very-low-density lipoprotein in suncus liver: an animal model of fatty liver.
We previously showed that fatty liver was easily induced in suncus by starvation and that the plasma level of apolipoprotein B (apo B) was very low. There are three possible explanations for the low level of apo B in the animals: low synthetic rate, low secretion rate, and rapid catabolism in the circulation of apo B. We measured post-heparin lipolytic activity (lipoprotein lipase activity), which plays a key role in the catabolism of apo B-containing lipoprotein, VLDL, and found no difference between rats and suncus. We also investigated the hepatic synthetic rate of apo B by liver perfusion studies. Newly synthesized apo B in the suncus liver was detected by immunoprecipitation and found to amount to 12.5% of that in rats. The secretion rate of VLDL in suncus, which was estimated by intravenous injection of Triton WR1339, was 13.8% of that in rats. These two results suggest that there is no major defect in the secretory process. We separated Golgi apparatus from rat and suncus livers, and found much fewer lipoprotein particles in suncus than in rat Golgi apparatus. This evidence suggests that there is no defect in the lipolytic process or hepatic secretory process of apo B-containing lipoprotein, VLDL, but there may be a defect in the assembly process of VLDL and/or in the synthetic process of apo B in suncus. Such a defect may be one of the reasons for starvation-induced fatty liver in suncus.
Animals↗
Visceral fat accumulation and insulin resistance are important factors in nonalcoholic fatty liver disease.
BACKGROUND: Nonalcoholic fatty liver diseases are often associated with obesity, insulin resistance, and excessive visceral fat accumulation. The aims of this study were (1) to evaluate the relationship between the severity of fatty liver and visceral fat accumulation in nonalcoholic fatty liver diseases, and (2) to investigate the relationships of fatty liver with biochemical data and insulin resistance. METHODS: One hundred twenty-nine subjects (63 women) with fatty liver diagnosed by ultrasonography were enrolled. Subjects positive for hepatitis B virus, hepatitis C virus, or autoimmune antibodies and those whose alcohol intake was over 20 g/day were excluded. The visceral fat area at the umbilical level and the liver-spleen ratio were evaluated by computed tomography. RESULTS: The severity of fatty liver evaluated by ultrasonography showed a significant positive relationship with the visceral fat area and waist circumstance (fatty liver severity: mild, 92.0 +/- 30.9 cm(2); moderate, 122.1 +/- 32.6 cm(2); severe, 161.0 +/- 48.4 cm(2); P < 0.0001). The visceral fat area and liver-spleen ratio were negatively correlated (r = -0.605, P < 0.0001). The severity of fatty liver showed strong positive relationships with serum aspartate aminotransferase, alanine aminotransferase, fasting plasma glucose, fasting plasma insulin, and insulin resistance. The severity of fatty liver was positively related to the visceral fat area in 49 nonobese subjects (body mass index <25). CONCLUSIONS: The severity of fatty liver was positively correlated with visceral fat accumulation and insulin resistance in both obese and nonobese subjects, suggesting that hepatic fat infiltration in nonalcoholic fatty liver disease may be influenced by visceral fat accumulation regardless of body mass index.
Adipose Tissue↗
Usefulness of redox tolerance test in evaluating fatty liver.
BACKGROUND/AIMS: In living-related liver transplantation, fatty liver should be exactly detected in the healthy donor with noninvasive measurement before the surgery. The study aimed to investigate the usefulness of redox tolerance test in diagnosing fatty liver. METHODOLOGY: The subjects were 32 patients who underwent an abdominal surgery. They did not show any abnormal values in biochemical evaluations, nor had they diabetes. Under informed consent, liver specimens were obtained intraoperatively, and the subjects were divided into three groups according to the degree of hepatic fatty deposit: group A has fatty deposits at less than 10% of hepatocytes (n = 12), group B showed the deposits at 10-30% (n = 10), group C has the deposits of more than 30% (n = 10). Before the surgery, redox tolerance test was performed as follows; arterial blood samples were obtained successively at 75 g oral glucose load over a 120-min period, and the arterial ketone body ratio and blood glucose level were determined. The ratio of increased arterial ketone body ratio (AKBR) to increased blood glucose (BG) level (100 x delta AKBR/delta BG) was calculated as redox tolerance index. RESULTS: After fasting state, arterial ketone body ratio and blood glucose level did not differ among the three groups. However, the values of redox tolerance index in groups B (0.73 +/- 0.08) and C (0.46 +/- 0.04) were significantly lower than those in group A (1.85 +/- 0.31). CONCLUSIONS: The redox tolerance test was exceedingly sensitive indicator for objectively diagnosing the fatty liver.
3-Hydroxybutyric Acid↗
[The effect of ethanol on the fatty liver in Zucker fatty rat].
Explore the source record for details and available documents.
Animals↗
Leptin, insulin resistance, and liver fibrosis in human nonalcoholic fatty liver disease.
BACKGROUND/AIMS: Data from animal models of fibrosis and fatty liver suggest that leptin may mediate the profibrogenic responses in the liver, but the association of leptin and liver fibrosis in human nonalcoholic fatty liver disease (NAFLD) remains undefined. We aimed at determining the relation between leptin and liver fibrosis in human NAFLD. METHODS: Human plasma leptin and several indicators of insulin resistance were measured in 88 NAFLD patients and matched controls. RESULTS: Leptin levels were significantly greater in patients with more advanced fibrosis (P = 0.005). By multivariate analysis, the significant association between leptin and fibrosis was abolished (adjusted P = 0.3) when controlling for confounders including age, gender, BMI, diabetes and insulin resistance. Only age (adjusted P = 0.006) and insulin sensitivity (adjusted P = 0.04) correlated significantly with fibrosis stage. A second liver biopsy was performed in 39 out of the 88 patients at 27.9 +/- 16 months. Leptin levels were not significantly different between patients who had fibrosis progression (n = 10) and those who did not (n = 29). CONCLUSIONS: In human NAFLD, no relationship between leptin levels and fibrosis stage was demonstrated. The correlation of leptin and fibrosis severity seems to be an indicator of the factors that determine leptin production.
Adult↗
Apoptosis and fibrosis in non-alcoholic fatty liver disease.
Nonalcoholic fatty liver disease is becoming an increasingly common medical problem in the developed countries which, unfortunately, still is associated with the lack of any effective treatment. However, recent data favor a model in which a pathologically increased rate of hepatocytic apoptosis and the subsequent induction and upregulation of inflammation and fibrosis in the liver provide both a rationale for the pathogenesis of nonalcoholic fatty liver disease, as well as a clue for designing first effective therapeutic strategies. In order to illuminate this context, this article focuses on the pathogenesis and possible new therapeutic options in nonalcoholic fatty liver disease.
Animals↗
Ethanol-induced fatty liver: the requirement of ethanol metabolism for the development of fatty liver.
Explore the source record for details and available documents.
Animals↗
Tumor necrosis factor and its potential role in insulin resistance and nonalcoholic fatty liver disease.
Nonalcoholic fatty liver disease (NAFLD) is a spectrum of hepatic pathology that resembles alcohol-induced fatty liver disease(AFLD), but which develops in individuals who are not heavy drinkers. In people, NAFLD is associated strongly with obesity,insulin resistance, and dysmetabolic syndrome, but the exact mechanisms that promote liver disease in this clinical context remain poorly understood. The proinflammatory cytokine, funor necrosis factor alpha is known to be a key mediator of AFLD. This article discusses clinical and experimental evidence that tumor necrosis factor plays a role in the pathogenesis of insulin resistance syndromes, including nonalcoholic fatty syndromes, including nonalcoholic fatty liver disease.
Animals↗
Correlation between intrasinusoidal neutrophilic infiltration and ceroid-lipofuscinosis in alcoholic liver fibrosis with or without fatty change: clinicopathological comparison with nutritional fatty liver.
A histopathological study was conducted on alcoholic liver fibrosis with fatty change (21 cases) and alcoholic liver fibrosis without fatty change (18 cases) in comparison with nutritional fatty liver (27 cases). The diagnoses of alcoholic liver fibrosis groups were clinically fulfilled according to the criteria established by the Alcohol and Liver Research Group (Chief: Professor Takeuchi) of the Ministry of Education of Japan. Histological diagnosis of alcoholic liver fibrosis with fatty change was based on moderate and/or greater fatty metamorphosis of the hepatic lobules, alcoholic liver fibrosis without fatty change on a lesser degree of fatty metamorphosis than alcoholic liver fibrosis with fatty change, and nutritional fatty liver on clinicopathological features. All 66 cases were negative for viral markers of hepatitis B surface antigen and anti-hepatitis C virus in serum. Intrasinusoidal neutrophil infiltrations were significant in cases of alcoholic liver fibrosis groups more often than in cases of nutritional fatty liver. The degree of intrasinusoidal neutrophil infiltration in cases of alcoholic liver fibrosis groups was higher in cases who had last consumed alcohol recently, compared with those with longer abstinence. In alcoholic liver fibrosis with fatty change and nutritional fatty liver groups, mild-to-moderate degrees of ceroid-lipofuscinosis were recognized, but both fatty change and ceroid-lipofuscinosis were decreased according to the deterioration of fibrotic changes in alcoholic liver fibrosis with fatty change cases. On the other hand, it is significant that the frequency of ceroid-lipofuscinosis in alcoholic liver fibrosis without the fatty change group was lower than those of the alcoholic liver fibrosis with fatty change and nutritional fatty liver groups. Distribution of ceroid-lipofuscinosis has a tendency to be recognized around the central zone (zone III) of alcoholic liver fibrosis with fatty change cases with mild fibrosis, as in nutritional fatty liver cases, and the ceroid-lipofuscinosis disperses with the progression of fibrosis. These results suggest that fibrosis and fatty droplet deposition lead to microvascular heterogeneity. Therefore, the degree and distribution of fatty droplets, ceroid-lipofuscinosis, and intrasinusoidal neutrophil infiltration differ, depending on the etiology of fatty liver, and are an important histopathological barometer in cases of alcoholic liver fibrosis with fatty change and alcoholic liver fibrosis without fatty change, thus indicating the degree of fibrosis and the period since last alcohol intake.
Adult↗
Nonalcoholic fatty liver disease and liver transplantation.
Nonalcoholic fatty liver disease affects a substantial proportion of the general population worldwide. This high prevalence of nonalcoholic fatty liver disease has important consequences in the donor selection process for liver transplantation, and in the posttransplant period given the high recurrence rate of disease. This paper reviews the prevalence of nonalcoholic fatty liver disease, its progressive potential, and the implications of this liver condition in both the pre- and post-liver transplantation setting.
Disease Progression↗
The association between acute fatty liver of pregnancy and fatty acid oxidation disorders.
Acute fatty liver of pregnancy is a relatively rare but potentially fatal liver disorder of late pregnancy. Recent advances in molecular diagnostic procedures provide evidence of a genetic basis for this condition and a link to offspring disorders in fatty acid oxidation. This relationship implies the need for genetic testing and follow-up of at-risk women and their neonates.
Acute Disease↗
Valproate therapy and nonalcoholic fatty liver disease.
Nonalcoholic fatty liver disease was defined recently as another symptom of insulin resistance. Continuous therapy with valproate can result in increased body weight and insulin resistance, but no data are yet available on a possible relationship between valproate and nonalcoholic fatty liver disease. We here demonstrate in abdominal ultrasound investigations that characteristics of fatty liver disease were present in 61% of valproate-treated patients as compared with 23% receiving carbamazepine therapy.
Adolescent↗
Advances in the understanding and treatment of nonalcoholic fatty liver disease.
Nonalcoholic fatty liver disease (NAFLD) is a well recognised form of chronic liver disease that has recently gained greater recognition. Originally described in the late 1950s, NAFLD is currently considered the leading cause of abnormal liver enzyme levels in the US, closely paralleling the increase in obesity and diabetes mellitus. NAFLD has a worldwide distribution, affecting both adults and children, and typically is seen in association with obesity, diabetes, hypertension and hypertriglyceridaemia. Most patients are asymptomatic and usually present with mild elevations in aminotransferases. The natural history of NAFLD is not clearly defined but progression to cirrhosis and end-stage liver disease is well recognised in some patients. The accumulation of hepatic steatosis is thought to occur initially, primarily through hepatic and peripheral insulin resistance, which leads to altered glucose and free fatty acid metabolism. The progression from simple fatty liver to more severe forms of NAFLD (nonalcoholic steatohepatitis and cirrhosis) is much less clear but evidence suggests that oxidative stress may preferentially enhance proinflammatory cytokines, which leads to cellular adaptations and dysfunction followed by development of inflammation, necrosis and fibrosis. Therapeutic modalities remain limited and are largely focused on correcting the underlying insulin resistance or reducing oxidative stress. However, at the present time, there are several limitations to the current potential therapies, mainly because of the lack of large-scale, prospective, randomised studies, as well as clearly defined histological endpoints. Ultimately, the future for potential therapeutic modalities to treat this disease are quite promising, but further research is needed to clearly demonstrate which therapy or therapies will be effective at eliminating fatty liver disease and its potential complications.
Antioxidants↗
Regulation of pathways of extramitochondrial fatty acid oxidation and liver fatty acid-binding protein by long-chain monocarboxylic fatty acids in hepatocytes. Effect of inhibition of carnitine palmitoyltransferase I.
The regulation of the extramitochondrial fatty acid oxidation pathways located in the peroxisomes and the endoplasmic reticulum is not fully understood. Although both long-chain dicarboxylic fatty acids, which are poorly metabolized in hepatocytes, and non-beta-oxidizable fatty acid analogs induce peroxisomal beta-oxidation and liver fatty acid-binding protein (L-FABP) by a pretranslational mechanism, monocarboxylic long-chain fatty acids, which are rapidly esterified and oxidized, do not. To establish whether impaired utilization and, hence, sustained intracellular levels of monocarboxylic long-chain fatty acids increase their efficacy as inducers, the effect of oleic acid on cytochrome P-450 4A1, peroxisomal beta-oxidation, and L-FABP during inhibition of mitochondrial beta-oxidation was determined. In primary hepatocyte cultures, oleic acid had no inducing effect, but in the presence of 2-tetradecylglycidic acid (TDGA), an inhibitor of carnitine palmitoyltransferase I, it induced P-450 4A1, peroxisomal beta-oxidation, and L-FABP pretranslationally. An increase in peroxisomal beta-oxidation was also noted in the presence of etomoxir, another inhibitor of carnitine palmitoyltransferase I. Exposure of hepatocytes to TDGA for 1 h led to an expected decrease in incorporation of radiolabel from [1-14C]oleate into CO2 and water-soluble products. In contrast, long-term exposure to TDGA increased incorporation of [1-14C]oleate into oxidation products, most likely due to an adaptive induction of peroxisomal beta-oxidation. Both acute and long-term exposure of hepatocytes to TDGA decreased incorporation of oleic acid into triglycerides, an effect that may have contributed to the intracellular accumulation of fatty acids. These results provide support for a mechanism by which long-chain fatty acids or specific metabolites, including long-chain acyl-CoA esters and long-chain dicarboxylic acids, act as signals in the induction of P-450 4A1, peroxisomal beta-oxidation, and L-FABP under conditions in which long-chain fatty acids accumulate due to impaired entry into the mitochondrial beta-oxidation pathway.
Acyl-CoA Oxidase↗
Peritoneoscopic examination using intravenous administration of indocyanine green in the fatty liver.
Forty patients with fatty liver were studied by peritoneoscopic examination after intravenous administration of indocyanine green (ICG). Although diffuse or centrilobular steatosis was observed in both nonalcoholic and alcoholic fatty liver, periportal steatosis was seen only in alcoholic fatty liver. Vascular markings were more prominent in alcoholic fatty liver, especially in those with fibrosis, compared with nonalcoholic fatty liver. Fat was not stained with ICG. Unstained red patches, observed after ICG administration in both nonalcoholic and alcoholic fatty liver, were thought to be due to congestion in the former and to lobular inflammation as well as congestion in the latter. Acinar markings were indistinct in the fatty liver with fibrosis but became clearer after ICG administration.
Adolescent↗