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 775 records · Page 43Linked to original sources
PubMed2005

Association between plasma interleukin-18 levels and liver injury in chronic hepatitis C virus infection and non-alcoholic fatty liver disease.

There is significant upregulation of interleukin-18 (IL-18) expression in viral infectious diseases and in some chronic hepatic diseases, especially (i) hepatitis C virus (HCV) infection, (ii) HCV infection with persistently normal ALT levels (PNAL), and (iii) non-alcoholic fatty liver disease (NAFLD). The aim of this study was a better understanding of the implications of plasma IL-18 levels in the above-mentioned liver diseases. Thirty-four patients with HCV infection, 13 with NAFLD, and 10 controls were enrolled. The HCV-RNA and HCV-genotypes and the serum or plasma levels of IL-18, aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (gamma-GT), alkaline phosphatase, total cholesterol, triglycerides, alpha(1)-fetoprotein, and ferritin were evaluated. Patients with HCV showed higher levels of IL-18 than the NAFLD patients (p <0.01) and the controls (p <0.005). Patients with NAFLD showed higher values of body mass index and liver disease parameters, compared to HCV-infected subjects or controls. These data confirm previous reports of enhanced expression of IL-18 in patients with HCV and NAFLD, compared to healthy subjects, and suggest that IL-18 is important as a marker of liver diseases.

Alanine Transaminase↗
PubMed1987

Liver fatty acid binding protein is the mitosis-associated polypeptide target of a carcinogen in rat hepatocytes.

Hepatocytes in normal rat liver were found previously to contain a cytoplasmic 14,000-dalton polypeptide (p14) that is associated with mitosis and is the principal early covalent target of activated metabolites of the carcinogen N-2-fluorenylacetamide (2-acetylaminofluorene). The level of immunohistochemically detected p14 was low when growth activity of hepatocytes was low, was markedly elevated during mitosis in normal and regenerating livers, but was very high throughout interphase during proliferation of hyperplastic and malignant hepatocytes induced in rat liver by a carcinogen (N-2-fluorenylacetamide or 3'-methyl-4-dimethylaminoazobenzene). We report here that p14 is the liver fatty acid binding protein. The nucleotide sequence of p14 cDNA clones, isolated by screening a rat liver cDNA library in bacteriophage lambda gt11 using p14 antiserum, was completely identical to part of the sequence reported for liver fatty acid binding protein. Furthermore, the two proteins shared the following properties: size of mRNA, amino acid composition, molecular size according to NaDodSO4 gel electrophoresis, and electrophoretic mobilities in a Triton X-100/acetic acid/urea gel. Their pI values overlapped in 2-dimensional isoelectric focusing/NaDodSO4 gel electrophoresis and showed the same response to delipidation. Either polypeptide reacted with and blocked the antiserum raised against the other polypeptide. The two polypeptides bound oleic acid similarly. Finally, identical elevations of cytoplasmic immunostain were detected specifically in mitotic hepatocytes with either antiserum. The collected findings are suggestive that liver fatty acid binding protein may carry ligands that promote hepatocyte division and may transport certain activated chemical carcinogens.

2-Acetylaminofluorene↗
PubMed2025

Newly identified single-nucleotide polymorphism associated with the transition from nonalcoholic fatty liver disease to liver fibrosis: results from a nested case-control study in the UK biobank.

BACKGROUND: Genetic factors may have a significant influence on the likelihood of liver fibrosis in individuals with nonalcoholic fatty liver disease (NAFLD). The present study was conducted to explore how single-nucleotide polymorphism (SNP) impacts the development of fibrosis in those suffering from NAFLD. MATERIALS AND METHODS: Utilizing the UK Biobank dataset, we conducted a nested case-control analysis among NAFLD participants, defining the case group as those with liver fibrosis and cirrhosis during follow-up. For our in vitro investigations, we employed the LX-2 human hepatic stellate cell line. Our procedures included cultivating these cells, employing SAMM50-rs2073080 plasmid techniques to enhance the expression of recently discovered SNPs, and conducting biochemical assays. To quantify gene expression, we used real-time PCR with fluorescence detection. RESULTS: The study analyzed data from 5467 participants (1094 cases and 4373 controls). Genome-wide association analysis identified nine significant loci, including the novel rs2073080 variant, strongly associated with NAFLD-associated hepatic fibrosis. In vitro TGF-&#x3b2; modeling revealed significant upregulation of &#x3b1;-SMA and COL1A1, confirming model effectiveness. Oxidative stress markers like elevated malondialdehyde (MDA) and reduced catalase (CAT) and superoxide dismutase (SOD) levels indicated liver damage in the TGF-&#x3b2; group. SAMM50-rs2073080 was upregulated in the NAFLD-associated fibrosis model. In vitro experiments on LX-2 cells showed that SAMM50-rs2073080 overexpression led to increased fibrosis, as indicated by higher cellular MDA levels and lower CAT and SOD levels, compared to the vector group. CONCLUSION: Our research highlights a significant association of SAMM50-rs2073080 with the progression of NAFLD to hepatic fibrosis, and the in vitro experiments further corroborated these findings.

Humans↗
PubMed1972

Fatty liver induction: inverse relationship between hepatic neutral lipid accumulation and dietary polyunsaturated fatty acids in orotic acid-fed rats.

The levels of hepatic neutral lipids in the orotic acid-fed rat were inversely related to the dietary levels of polyunsaturated fatty acids, as in the choline-deficient rat. Hepatic microsomal protein and phospholipid and total hepatic phospholipid were increased in orotic acid-induced fatty livers. The increase in phospholipid was largely restricted to the phosphatidylethanolamines.

Aniline Compounds↗
PubMed1984

Drug metabolism in diabetic subjects with fatty livers.

The effect of fatty degeneration of liver parenchyma on drug metabolism was investigated in 21 obese non-insulin-dependent diabetic subjects by measuring plasma antipyrine kinetics, hepatic cytochrome P-450, liver size and the extent of fatty infiltration. The hepatic drug metabolising capacity, as measured by total antipyrine clearance and the estimated total amount of cytochrome P-450, was at the same level as in non-diabetic control subjects with normal livers. Relative antipyrine clearance (per unit weight of liver) and cytochrome P-450 concentrations were significantly lower in the diabetics than in controls. The extent of fatty infiltration correlated poorly with the indices of drug metabolism. In non-insulin-dependent diabetics, slight to moderate hepatic fatty infiltration, without more serious structural distortion interfering with hepatic blood flow or hepatocellular function, seems to have only a minor influence on drug metabolism.

Adult↗
PubMed2006

Prevention of fatty liver in transition dairy cows by subcutaneous injections of glucagon.

The main objective of this study was to test the extent to which injecting glucagon subcutaneously for 14 d beginning at d 2 postpartum would prevent fatty liver development in transition dairy cows. Twenty-four multiparous Holstein cows were fed 6 kg of cracked corn in addition to their standard diet during the last 30 d of a dry period to induce postpartum development of fatty liver. Glucagon at either 7.5 or 15 mg/d or saline (control) was injected subcutaneously 3 times daily for 14 d beginning at d 2 postpartum. Glucagon at 15 mg/ d prevented liver triacylglycerol accumulation in postpartum dairy cows. Glucagon at 7.5 mg/d showed potential for fatty liver prevention. Glucagon increased concentration of plasma glucose and insulin and decreased plasma nonesterified fatty acid concentrations. No effects of glucagon were detected on plasma beta-hydroxybutyrate concentrations. Glucagon affected neither feed intake nor milk production. Moreover, milk composition was not altered by glucagon. Milk urea N concentrations decreased, and plasma urea N concentrations tended to decrease during glucagon administration, indicating that glucagon may improve protein use. Liver glycogen concentrations were not affected by glucagon. No significant differences in body condition scores were detected among treatments throughout the study. These results indicate that subcutaneous glucagon injections can prevent fatty liver in transition dairy cows without causing major production and metabolite disturbances.

Acetoacetates↗
PubMed1989

[A case of focal fatty liver difficult to distinguish from the liver metastasis of rectal cancer on CT].

The CT findings of focal fatty liver were previously described as follows, 1) nonspherical shape, 2) indistinct border, 3) absence of mass effect and 4) subsegmental appearance. We presented a case of focal fatty liver with spherical shape and distinct border, resembling the findings of liver tumor. In this case we could not rule out the liver metastasis from rectal cancer to the end. CT value and follow up examination are very useful to establish the proper diagnosis.

Adenocarcinoma↗
PubMed1986

Serum alanine aminotransferase to aspartate aminotransferase ratio and degree of fatty liver in morbidly obese patients.

We evaluated the change in serum alanine aminotransferase (ALT; EC 2.6.1.2) to serum aspartate aminotransferase (AST; EC 2.6.1.; ALT/AST) ratio with the degree of fatty liver in morbidly obese patients. A total of 31 patients were included in the study. Fatty liver was graded as 0 to 4+. The mean and SD of AST and ALT were not significantly different between groups of patients with various grades of fatty liver. There was, however, a significant correlation between the ALT/AST ratio and the degree of fatty infiltration of the liver. This, we believe, implies damage mainly to the plasma membrane allowing loss of cytoplasmic enzymes rather than loss of mitochondrial enzymes.

Adult↗
PubMedDate not supplied

Metastases in fatty liver: appearance on conventional spin-echo, fast-spin-echo, and echo-planar T2-weighted MR images.

A 71-year-old woman with liver metastases from colon adenocarcinoma in a severe fatty liver underwent T2-weighted MR imaging with conventional spin-echo (CSE), breath-hold fast-SE (BH-fast-SE), respiratory-triggered fast-SE (RT-fast-SE), and multishot SE echo-planar (SE-EP) techniques. CSE and SE-EP T2-weighted images showed the metastases as areas of high signal intensity. In contrast, RT-fast-SE and BH-fast-SE images showed them as areas of low signal intensity. Metastatic tumors in severe fatty liver can be shown as low signal-intensity areas with T2-weighted MR imaging using fast-SE sequences without use of the fat-suppression technique.

Adenocarcinoma↗
PubMed2004

p53 involvement in the pathogenesis of fatty liver disease.

Obesity is a major health problem in industrialized societies, and fatty liver disease (hepatic steatosis) is common in obese individuals. Oxidative stress originating from increased intracellular levels of fatty acids has been implicated as a cause of hepatocellular injury in steatosis, although the precise mechanisms remain to be elucidated. p53, widely known as a tumor suppressor, has been shown often to be activated in stressed cells, inducing cell cycle arrest or death. Here we demonstrate that p53 is involved in the molecular mechanisms of hepatocellular injury associated with steatosis. We found that p53 in the nucleus is induced in the liver from two mouse models of fatty liver disease, ob/ob and a transgenic mouse model that overexpresses an active form of sterol regulatory element-binding protein-1 in the liver (TgSREBP-1), the one with obesity and the other without obesity. This activation of the p53 pathway leads to the elevation of p21 mRNA expression, which can be considered an indicator of p53 activity, because ob/ob mice lacking p53 generated by targeting gene disruption exhibited the complete restoration of the p21 elevation to wild type levels. Consistent with these results, the amelioration of hepatic steatosis caused by Srebp-1 gene disruption in ob/ob mice lowered the p21 expression in a triglyceride content-dependent manner. Moreover, p53 deficiency in ob/ob mice resulted in a marked improvement of plasma alanine aminotransferase levels, demonstrating that p53 is involved in the mechanisms of hepatocellular injury. In conclusion, we revealed that p53 plays an important role in the pathogenesis of fatty liver disease.

Animals↗
PubMed2002

In situ detection of lipid peroxidation and oxidative DNA damage in non-alcoholic fatty liver diseases.

BACKGROUND/AIMS: Although oxidative stress is an important candidate in the pathogenesis of non-alcoholic fatty liver disease (NAFLD), the localization and pathological significance of oxidative stress-induced cellular damage in NAFLD remains unclear. METHODS: Hepatic expression of 4-hydroxy-2'-nonenal (HNE) and 8-hydroxydeoxyguanosine (8-OHdG), as reliable markers of lipid peroxidation and oxidative DNA damage, respectively, was immunohistochemically investigated in NAFLD and the results were compared with histological findings. RESULTS: While no HNE adducts were observed in control livers, they were frequently detected in NAFLD. In NASH, the localization of the adducts was in the cytoplasm of sinusoidal cells and hepatocytes with a predominance in zone 3. The grade of necro-inflammation as well as the stage of fibrosis significantly correlated with the HNE index. Regarding 8-OHdG, although no 8-OHdG expression was observed in normal liver and only a few in fatty liver, 11 of 17 cases (64.7%) with NASH exhibited nuclear expression of 8-OHdG in hepatocytes and sinusoidal cells in areas of active inflammation. The 8-OHdG index significantly correlated with the grade of necro-inflammation. CONCLUSIONS: Oxidative cellular damage occurs frequently in livers with NAFLD and may be associated with some clinico-pathological features of NAFLD including liver fibrosis and possibly, hepatocarcinogenesis.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2006

Characterization of benign hepatic tumors arising in fatty liver with SonoVue and pulse inversion US.

BACKGROUND: We describe the spectrum of contrast-enhancement patterns of benign hepatic tumors arising in fatty liver on contrast-enhanced ultrasound (US). METHODS: Sixteen patients (12 women and four men) with 27 benign hepatic tumors (17 hemangiomas, eight focal nodular hyperplasias, and two hepatocellular adenomas) arising in fatty liver underwent baseline and pulse inversion US after administration of SonoVue. Two experienced radiologists evaluated baseline echogenicity and dynamic enhancement pattern of each lesion in comparison with adjacent liver parenchyma. RESULTS: After administration of SonoVue, in the arterial phase 13 of 17 hemangiomas showed peripheral globular enhancement and one showed a rim of peripheral enhancement, followed by progressive centripetal fill-in, which was complete in 10 of 14 cases and incomplete in four. Three of 18 hemangiomas showed rapid and complete fill-in in the arterial phase. Eight of eight focal nodular hyperplasias became hyperechoic in comparison with adjacent liver parenchyma in the arterial phase and slightly hyperechoic or isoechoic in the portal venous and delayed phases. Both adenomas showed strong arterial contrast enhancement that became less intense in the portal venous and delayed phases. CONCLUSION: Contrast-enhanced US after administration of SonoVue enables depiction of typical contrast-enhancement patterns in most benign hepatic tumors arising in fatty liver, thus providing useful clues for characterization.

Adenoma, Liver Cell↗
PubMed2005

Oxidative injury in rat fatty liver exposed to ischemia-reperfusion is modulated by nutritional status.

BACKGROUND AND AIMS: Oxidative stress contributes to ischemia-reperfusion injury in fatty livers. This study aimed to determine whether glycogen depletion influences this oxidative injury and whether the administration of glucose can be protective. METHODS: Rats with choline deficiency-induced fatty liver underwent hepatic ischemia-reperfusion. Experimental groups: (1) fed rats; (2) 18 h fasted rats; (3) 18 h fasted rats supplemented with glucose prior to surgery. The thiobarbituric acid-reactive substances, protein carbonyls and total glutathione concentrations were measured in liver tissue and isolated mitochondria as parameters of oxidative stress before and after ischemia and during reperfusion. The mitochondrial F1-ATPase content and the serum alanine transaminase were also determined. RESULTS: With respect to fed rats, fasted rats exhibited an increased oxidative injury in both liver tissue and isolated mitochondria throughout the experiment with the only exception of thiobarbituric acid-reactive substances, which were not affected by the nutritional status in liver tissue. Fasted rats showed a significantly lower F1-ATPase content and higher alanine transaminase levels. Glucose supplementation significantly reduced the fasting-associated exacerbation of oxidative stress and liver injury and the F1-ATPase exhaustion. CONCLUSIONS: These data indicate that the pre-existing hepatic glycogen content modulates the oxidative damage in rat fatty livers exposed to ischemia-reperfusion injury and that the energetic substrate supplementation may represent a clinically feasible protective strategy.

Alanine Transaminase↗
PubMed2002

Non-alcoholic fatty liver disease: an overview.

Non-alcoholic fatty liver disease (NAFL) includes a spectrum of clinicopathological conditions with increasing prevalence in the developed world. Although steatosis alone seems to have a benign course, those patients with the diagnosis of non-alcoholic steatohepatitis (NASH) can have a progressive course. Additionally, there is now evolving, indirect evidence that some of the patients with cryptogenic cirrhosis may be the result of 'burned-out' NASH. Although NAFL and NASH are associated with insulin-resistance syndrome, some patients with NAFL may have no obvious risk factors. Despite preliminary data from a number of pilot studies, no established therapies can be offered to patients with NASH. Over the next few years, a number of exciting research projects dealing with the epidemiology as well as the pathogenesis of NAFL are expected to be completed. It is anticipated that, through a better understanding of NAFL, more effective treatment protocols can be developed targeting only those patients with NASH that are at the highest risk for progression to cirrhosis and liver failure.

Chronic Disease↗