Search PubMed⌕ Search

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.

At least 1,063 records · Page 59Linked to original sources

[Fatty liver quantification with line scan echo planar spectroscopic imaging (LSEPSI)].

INTRODUCTION: Although fatty infiltration of liver is a benign process that generally results from chronic alcohol uptake or obesity, such lifestyle factors may lead to chronic disease. Measuring the fat concentration in liver may therefore prove useful in assessing disease status. In this study, we report the usefulness of line scan echo planar spectroscopic imaging (LSEPSI) for this problem. METHODS: Rapid successive column sampling was accomplished using orthogonal slice-selective 90 degrees and 180 degrees pulses and echo planar spectral/spatial encodings. Phantom and clinical studies of 13 patients suspected of having fatty liver were carried out with LSEPSI. Estimated fat fractions obtained with LSEPSI were compared with ultrasound findings. RESULTS: The results showed a good correlation between the actual fat content of phantoms and the estimated fat fraction obtained with LSEPSI (r = 0.95). In the clinical study, the estimated fat fraction tended to rise as the US grade of fatty liver increased. DISCUSSION: LSEPSI is largely free from T1 and T2 relaxation owing to its infinite TR and minimal T2 weighting. Thus, there is no need for relaxation analysis. In addition, the lack of phase encoding reduces motion-related ghosting artifacts. Rapid fat/water spectral quantification of liver with this technique is useful for fatty liver assessment in a clinical setting.

Adult↗

[Changes in lipoglycoprotein metabolism in toxic fatty liver].

BACKGROUND: A number of agents that produce liver injury also cause the accumulation of an abnormal amount of fat, predominantly triglycerides (TGs) in the parenchymal cells. Fatty liver (FL) is the result of an hepatocyte imbalance between the rate of synthesis and output of TGs into the plasma. TGs are not secreted as such, but combined with a glycoprotein moiety, and particularly with the very low density lipoproteins (VLDLs). This fraction is involved in the transport of hepatic TGs to extrahepatic tissues. FL can be induced by either acute or chronic administration of ethanol (EtOH), and/or several haloalkanes (carbon tetrachloride, CCl4; 1.2-dichloroethane, DCE; 1.1.2.2-tetrachloroethane, TTCE), both in laboratory animals and in man. Since the pathogenesis of this disease is a crucial problem, as yet undefined, the purpose of this article is to summarize the studies which have unraveled some of the mechanisms involved in FL, particularly the role played by impaired lipoglycoproteins (LGP) metabolism in rat liver. DISCUSSION: An important element in the pathogenesis of EtOH- and haloalkanes-induced FL is the impairment of hepatic secretion of VLDLs, which occurs soon after poisoning. Various steps of the secretory pathway are probably involved in the expression of such damage. The intoxication of rats with these xenobiotics leads to an early impairment of the hepatocyte system responsible for terminal glycosylation and maturation of LGP at the level of three different subfractions (F1, F2 and F3) of purified Golgi apparatus (GA). The earliest functional change is a block of LGP transit through the GA cisternae and vesicles, both in isolated hepatocyte model and in the whole animal. The glycosylation of LGP is a multistep process which starts in the rough endoplasmic reticulum (RER), and comes to its end in the GA. Dolichols (Dol) are a family of long-chain polyisoprenoid alcohols, present either as neutral free-Dol and dolichyl-phosphate (Dol-P). The latter acts as a glycosyl carrier across the RER membranes in the initial steps of LGP biosynthesis. Nearly all the other reactions occur in GA, where free-Dol have a role either in terminal LGP processing or in their secretion into the blood stream. Several investigations indicated that both EtOH and haloalkanes (CCl4, DCE, and TTCE) may selectively and precociously impair the total microsomes (TM) and GA pool of Dol, particularly in F1. Lipid peroxidation appears to be the fundamental mechanism involved. CONCLUSIONS: Such results, obtained in several works, point out a key role played in FL by selective impairment of MT and GA processes which provide for the synthesis, maturation and release of hepatic LGP.

Animals↗

[Quantitative diagnosis of fatty liver using mask cover of CT image].

OBJECTIVES: To explore a non-invasive approach in detecting the degree of fatty infiltration of fatty liver. METHODS: The Liver and Spleen were scanned by GE 3000I CT machine with data processing functions. Based on the areas of fatty infiltration figured out by the mask cover, we calculated the proportion of areas infiltrated by fatty (index of fatty infiltration) and compared with the results shown in the liver biopsy. The liver functions were measured by the biochemical analysis machines. RESULTS: The average index of fatty infiltration was significantly correlated with the liver function and the degree of fatty infiltration detected by the liver biopsy. CONCLUSION: The mask cover of CT image is a reliable non-invasive approach for quantitative diagnosis of fatty liver. It is better than the liver biopsy especially for the focal fatty liver.

Adolescent↗

Characterization of the gut phageome and functional genes carried by phages in laying hens with fatty liver hemorrhagic syndrome.

BACKGROUND: The gut microbiota is closely associated with the development of fatty liver hemorrhagic syndrome (FLHS); however, the function of its viral component, particularly bacteriophages, remains poorly understood. This study compared clinical parameters and the cecal phageome between 30-week-old (W30) and 50-week-old (W50) laying hens to characterize gut phages in the context of this metabolic disorder. RESULTS: Clinical analysis revealed that the W50 group exhibited typical FLHS, accompanied by elevated serum liver function and lipid markers (P&#x2009;<&#x2009;0.05). Functional prediction of the gut microbiota suggested a reduced lipid-metabolic capacity in W50 compared to the W30 group. A total of 20,274 phage genomes were identified from the two groups. These phages were primarily classified into 67 viral families, including Salasmaviridae, Herelleviridae, Suoliviridae, Peduoviridae, Crevaviridae, and Casjensviridae. The families Druskaviridae, Felixviridae, and Stanwilliamsviridae were uniquely detected in the W50 group. The phage community structure differed significantly between groups, with both phage diversity and richness markedly lower in W50 (P&#x2009;<&#x2009;0.05). LEfSe analysis revealed that phage taxa such as Stegnyidae, Herpelidae, and Chasovidae were significantly enriched in the W50 group, whereas Crewdviridae, Salasmaviridae, and Castroviridae were predominantly enriched in the W30 group. Functional annotation showed that these phages encode numerous metabolism-related genes and carry antimicrobial resistance genes (ARGs) as well as virulence factor genes. Notably, the diversity of ARGs carried by W50 phages was significantly higher (P&#x2009;<&#x2009;0.05), and ARG-rank analysis indicated a greater potential risk to human health. CONCLUSIONS: This study provides the first characterization of the gut phageome associated with FLHS in laying hens and confirms that gut phages constitute an important reservoir of ARGs. These findings offer a new perspective for understanding the pathogenesis of this disease and its associated public health risks. Video Abstract.

Animals↗

The binding of natural and fluorescent lysophospholipids to wild-type and mutant rat liver fatty acid-binding protein and albumin.

Rat liver fatty acid-binding protein (FABP) is able to bind a wide range of non-polar anionic ligands, including lysophospholipids. In order to understand the nature of lysophospholipid interactions with liver FABP, the binding of natural lysophospholipids and two fluorescent analogues, N-(5-dimethylaminonaphthalenesulphonyl)-1-palmitoyl-sn-glycero-3- phosphoethanolamine (dansyl lysoPE) and 1-(O-[11-(5-dimethylaminonaphthalene-sulphonyl)amino]undecyl)-sn-glycero -3- phosphocholine (dansyl-C11-lysoPAF), has been investigated. The results confirmed the ability of liver FABP to bind lysophospholipids with KD values in the range of 1-2 microM, and a 1:1 binding stoichiometry was indicated. Binding of fluorescent lysophospholipids was enhanced with the FABP mutant, R122Q, possibly due to increased flexibility of the binding cavity as a result of reduced hydrogen-bonding constraints. The fluorescent lysophospholipids also bound to albumin, with KD values in the range 0.1-1.0 microM, and could be displaced by oleic acid. The fluorescence characteristics of the dansyl lysophospholipid analogue dansyl-C11-lyso-PAF suggested that this probe binds to the same site(s) on albumin as the fluorescent fatty acid probe 11-(5-dimethylaminonaphthalene-sulphonylamino)-undecanoic acid (DAUDA).

Albumins↗

Peritumoral spared area in fatty liver: correlation between opposed-phase gradient-echo MR imaging and CT arteriography.

BACKGROUND: The purpose of the present study was to evaluate the magnetic resonance findings of a spared area of fatty liver caused by hepatic tumors and clarify the etiology of this phenomenon by computed tomographic (CT) arteriography. METHODS: Six patients with hepatic tumors (metastases from colon cancer, n = 3; breast cancer, n = 2; hepatocellular carcinoma, n = 1) were examined. In-phase (IP) and opposed-phase (OP) T1-weighted spoiled gradient-echo images were obtained. CT during arterial portography (CTAP) and CT during hepatic arteriography (CTHA) were also performed. Pathologic confirmation was obtained in three patients with metastases from colon cancer. RESULTS: In all six patients, peritumoral ringlike or wedge-shaped hyperintense areas in relation to the tumor and the surrounding steatotic liver parenchyma were clearly visualized on OP images alone. This area appeared as a perfusion defect on CTAP and ringlike or wedge-shaped enhancement on CTHA. Pathologically, the peritumoral hyperintense areas on OP images were compatible with the spared area of fatty liver. CONCLUSION: A peritumoral spared area can be demonstrated with OP images. The etiology of the phenomenon is correlated with decreased portal flow and increased arterial flow in the peritumoral hepatic parenchyma.

Adult↗

Coordinate transcriptional repression of liver fatty acid-binding protein and microsomal triglyceride transfer protein blocks hepatic very low density lipoprotein secretion without hepatosteatosis.

Unlike the livers of humans and mice, and most hepatoma cells, which accumulate triglycerides when treated with microsomal triglyceride transfer protein (MTP) inhibitors, L35 rat hepatoma cells do not express MTP and cannot secrete very low density lipoprotein (VLDL), yet they do not accumulate triglyceride. In these studies we show that transcriptional co-repression of the two lipid transfer proteins, liver fatty acid-binding protein (L-FABP) and MTP, which cooperatively shunt fatty acids into de novo synthesized glycerolipids and the transfer of lipids into VLDL, respectively, act together to maintain hepatic lipid homeostasis. FAO rat hepatoma cells express L-FABP and MTP and demonstrate the ability to assemble and secrete VLDL. In contrast, L35 cells, derived as a single cell clone from FAO cells, do not express L-FABP or MTP nor do they assemble and secrete VLDL. We used these hepatoma cells to elucidate how a conserved DR1 promoter element present in the promoters of L-FABP and MTP affects transcription, expression, and VLDL production. In FAO cells, the DR1 elements of both L-FABP and MTP promoters are occupied by peroxisome proliferator-activated receptor alpha-retinoid X receptor alpha (RXRalpha), with which PGC-1beta activates transcription. In contrast, in L35 cells the DR1 elements of both L-FABP and MTP promoters are occupied by chicken ovalbumin upstream promoter transcription factor II, and transcription is diminished. The combined findings indicate that peroxisome proliferator-activated receptor alpha-RXRalpha and PGC-1beta coordinately up-regulate L-FABP and MTP expression, by competing with chicken ovalbumin upstream promoter transcription factor II for the DR1 sites in the proximal promoters of each gene. Additional studies show that ablation of L-FABP prevents hepatic steatosis caused by treating mice with an MTP inhibitor. Our findings show that reducing both L-FABP and MTP is an effective means to reduce VLDL secretion without causing hepatic steatosis.

Animals↗

Focal sparing of fatty liver in segment II associated with aberrant left gastric vein.

We present a patient with aberrant left gastric vein (LGV) that directly enters the posterior edge of segment II in the liver. The corresponding area was focally spared of fatty liver. We consider that this aberrant LGV contributed to the cause of focal sparing. This is the first report of the use of helical CT and Doppler ultrasound to depict the aberrant LGV that directly enters the liver.

Adult↗

Focal fatty liver in a heifer: utility of ultrasonography in diagnosis.

A 30-month-old Holstein heifer presented with a history of decreased appetite and respiratory signs. Sonographic examination of the liver incidentally revealed an area of increased echogenicity between the portal vein and the gallbladder. The lesion was nonspherical and had no mass effect or displacement of the adjacent vessels. Its boundaries, to the liver, were geographic. The liver specimen was histologically compatible with a diagnosis of focal fatty liver change (FFLC). The sonographic features of focal fatty infiltration of the liver are characteristic. Recognition of the ultrasonographic data is important to differentiate FFLC from other lesions.

Animals↗

[Occurrence of synchronous colorectal cancer metastasis in the cirrhotic or fatty liver].

AIM: Metastases from colorectal cancers rarely occur in injured livers, however this phenomenon has not been fully investigated in patients with different degree of liver damage. Therefore in this study we evaluated the incidence of synchronous hepatic metastases in patients with fatty or cirrhotic liver submitted to surgery for colorectal neoplasms. METHODS: Seven hundred and forty-seven patients undergoing surgical treatment for colorectal neoplasms were evaluated: the clinicopathological data of 171 patients with liver cirrhosis and 33 with fatty liver were compared to those of 543 patients without liver damage. RESULTS: Gender, age, type of operative procedures performed and histological grading were similar in patients with or without liver damage. In patients with liver cirrhosis the incidence of stage II tumour was greater, while stage IV tumours (P < 0.001) and nodal involvement were significantly lower than in patients with non injured or fatty liver (P < 0.02 and P < 0.001 respectively) . At the time of surgery, synchronous hepatic metastases were present in 32% of patients with normal liver, in 15% of patients with fatty liver (P < 0.02) and in 4.7% of patients with liver cirrhosis (P < 0.001). CONCLUSIONS: Results of our study show that synchronous hepatic metastases of colorectal cancer are less frequently observed in patients with fatty or cirrhotic liver than in patients with non injured liver, indicating that chronically damaged livers are protected from the spread of secondary cancers.

Aged↗

[Fatty liver disease and other complications of obesity].

Obesity induces many organic complications (somatic, metabolic and mechanical). The aims of this prospective study were to evaluate its complications in a group of thirty fat patients. Fatty liver disease, detected by echography is noted at 70% of patients. Clinically, it makes pains at the right side and seems favorized by an elevated BMI > 40 kg/m2, and diabetes, hypertriglyceridemiae, hypercaloric and hyperglucidic ration. 10% of our patients present stone bile duct associated to fatty liver disease.

Adolescent↗

Hepatic hemodynamics and oxygen consumption in alcoholic fatty liver assessed by organ-reflectance spectrophotometry and the hydrogen clearance method.

Hepatic blood flow and estimated hepatic oxygen consumption were studied in rats treated chronically with ethanol by organ-reflectance spectrophotometry and the hydrogen clearance method. In the withdrawal state from ethanol, the concentration of hemoglobin in the hepatic tissue (delta Er569-650), the estimated hepatic oxygen consumption (estimated VO2) and the regional liver blood flow decreased significantly in rats treated chronically with ethanol in comparison with their controls. On the other hand, there was no significant difference in the estimated oxygen saturation of the hepatic blood hemoglobin (estimated SO2) between both groups. That is, an increase in oxygen extraction, which was exhibited by a decrease in the estimated SO2, did not occur in rats treated chronically with ethanol in spite of a decrease in blood supply. Thus, in the withdrawal state from ethanol, both oxygen delivery to the liver and oxygen utilization in the liver were disturbed at the stage of alcoholic fatty liver.

Animals↗

Nonalcoholic fatty liver disease: a review of current understanding and future impact.

Nonalcoholic fatty liver disease (NAFLD), already the most common form of liver disease in the United States, can be expected to increase in prevalence and severity in parallel with national epidemics of obesity and type 2 diabetes. NAFLD is frequently associated with insulin resistance. While insulin resistance, and thereby hyperinsulinemia, are, in large part, metabolic consequences of obesity, the basis of diversity in severity and progression of inflammation and fibrosis is not known. Increased susceptibility to oxidative stress is likely to play a role. Several patient characteristics have been associated with more severe histological findings in patients with NAFLD, including type 2 diabetes, hypertension, age over 40 years, and higher transaminases. Liver biopsy is, however, required to accurately grade and stage NAFLD histologically. Although the natural history of NAFLD is relatively poorly defined, NAFLD is increasingly recognized as an important cause of decompensated liver disease. Weight reduction and improved insulin sensitivity are associated with improved biochemical and histological parameters of NAFLD. There are, however, no proven safe and efficacious pharmacological treatments for NAFLD.

Biopsy↗

Long-term prognosis of nonalcoholic fatty liver disease: is pharmacological therapy actually necessary?

BACKGROUND AND AIM: Nonalcoholic fatty liver disease (NAFLD) comprises a wide spectrum of liver injury, ranging from steatosis and steatohepatitis to cirrhosis. Reasons for the different natural course in individuals with NAFLD are still unclear. The aim of this study was to describe the natural course of disease in individuals with NAFLD who did not receive pharmacological therapy. METHODS: A total of 27 individuals with NAFLD (male/female ratio: 10/17, mean age 49.7 years) were prospectively enrolled. Management after diagnosis consisted of establishment of an appropriate diet and exercise (walking and jogging) program, treatment of associated metabolic conditions such as diabetes and dyslipidemia, and discontinuation of potentially hepatotoxic drugs if the patient was taking these. Liver tests were performed at diagnosis and at 3-month intervals during the follow-up period. Mean follow-up period was 43.3 months (range 36-49 months). RESULTS: From baseline to the end of the follow-up period, although there was no significant difference observed in terms of the mean body mass index, serum aminotransferase levels significantly improved (48.8+/-29.9 U/L to 31.6+/-16.0 U/L for aspartate aminotransferase [AST] and 66.3+/-38.3 U/L to 39.6+/-22.9 U/L for alanine aminotransferase [ALT]; P<0.05). No significant differences in platelet counts, serum albumin level or prothrombin time were observed (P>0.05). No patient developed signs of advanced liver disease during the follow-up period. CONCLUSION: A treatment strategy comprising diet, exercise and management of associated metabolic conditions is associated with improvement in aminotransferases among patients with NAFLD. Further investigation is needed to examine the long-term efficacy of this approach on liver histology and clinical outcomes.

Alanine Transaminase↗

A randomized controlled trial of metformin versus vitamin E or prescriptive diet in nonalcoholic fatty liver disease.

OBJECTIVES: Metformin proved useful in the treatment of nonalcoholic fatty liver disease (NAFLD), but its superiority over nutritional treatment and antioxidants has never been demonstrated. We aimed to compare the usefulness of metformin versus prescriptive diet or vitamin E. METHODS: In an open label, randomized trial, nondiabetic NAFLD patients were given metformin (2 g/day; n = 55) for 12 months. The control cases were given either vitamin E (800 IU/day; n = 28) or were treated by a prescriptive, weight-reducing diet (n = 27). Outcome measures were liver enzymes, insulin resistance (homeostasis model assessment), parameters of the metabolic syndrome, and histology. RESULTS: Aminotransferase levels improved in all groups, in association with weight loss. The effects in the metformin arm were larger (p < 0.0001), and alanine aminotransferase normalized in 56% of cases (odds ratio (OR) versus. controls, 3.11; 95% confidence interval (CI), 1.56-6.20; p= 0.0013). In multivariate analysis, metformin treatment was associated with higher rates of aminotransferase normalization, after correction for age, gender, basal aminotransferases, and change in body mass index (OR, 5.98; 95% CI, 2.05-17.45). Differences were maintained when the two control groups were separately analyzed. The distribution of positive criteria for the metabolic syndrome was reduced only in the metformin arm (p= 0.001, signed rank test). A control biopsy in 17 metformin-treated cases (14 nonresponders) showed a significant decrease in liver fat (p= 0.0004), necroinflammation, and fibrosis (p= 0.012 for both). No side effects were observed during metformin treatment. CONCLUSIONS: Metformin treatment is better than a prescriptive diet or vitamin E in the therapy of NAFLD patients receiving nutritional counseling. Limited histological data support an association between improved aminotransferases and biopsy findings, which require confirmation in a double-blind trial with appropriate statistical power based on liver histology.

Adult↗